Ascariasis in a child with recurrent gastrointestinal hemorrhage: case report and literature review

Background: Ascaris lumbricoides is one of the most common soil-transmitted helminth infections worldwide, particularly in tropical and subtropical regions with poor sanitation. While most cases are asymptomatic, heavy infections can lead to serious complications including intestinal obstruction, biliary colic, and pancreatitis. This article reports a case of melena in a 4-year-old child associated with ascariasis and explores the potential pathological mechanisms and management strategies through a comprehensive literature review.

Case description: A 4-year-old boy was admitted with a one-month history of cough, lethargy for 4 days, and coma lasting 10 h. He had been diagnosed with septic shock, severe pneumonia, acute respiratory failure, and multiple organ dysfunction syndrome (MODS) at a local hospital, where he received endotracheal intubation with mechanical ventilation, aggressive fluid resuscitation, and antimicrobial therapy before being transferred to our institution for further management. During hospitalization, he experienced recurrent melena, which required blood product transfusion to correct anemia. Further investigations eventually identified ascariasis as a potential underlying contributing factor. Melena in this patient was likely related to septic shock-induced coagulopathy or mucosal ischemia, rather than direct Ascaris injury. The patient was treated with albendazole, and ultimately made a full recovery and was discharged successfully.

Conclusions: Ascaris lumbricoides infection represents a rare yet critical associated factor in septic shock complicated by severe gastrointestinal bleeding in children. This case report and literature review demonstrate that successful management hinges on early identification of the parasitic infection coupled with timely anthelmintic therapy following hemodynamic stabilization. However, the severe clinical manifestations are often directly caused by secondary bacterial infections. Clinicians, particularly those in endemic regions, require heightened vigilance for this potential complication.

Introduction

Ascaris lumbricoides infection represents one of the most prevalent soil-transmitted helminthiasis globally, with an estimated 1.2 billion cases (40% pediatric) concentrated in resource-limited rural communities (1). Although most infected individuals remain asymptomatic, ascariasis has been identified as a significant cause of acute abdomen in children in endemic areas (2). Severe complications encompass mechanical intestinal obstruction, biliary tract invasion, pancreatitis and peritonitis represent the most frequent severe complications (3, 4). Gastrointestinal hemorrhage associated with ascariasis is exceptionally rare but can lead to fatal outcomes if not promptly recognized and managed. This case report and literature review aims to elucidate the clinical presentation, potential pathological mechanisms, and management strategies of this unusual complication.

Case presentation

A 4-year-old male patient was transferred to the Pediatric Intensive Care Unit of Chengdu Women's and Children's Central Hospital in December 2024. The patient originated from a rural village in Liangshan Prefecture, Sichuan Province, and frequently played barefoot outdoors. He had no history of chronic diseases, surgeries, or drug/food allergies, and had completed all age-appropriate vaccinations. Family history was non-contributory, with no evidence of coagulation disorders, genetic diseases, or gastrointestinal malignancies.

On admission, the patient presented with a chronic ill appearance and moderate malnutrition, with a weight of 16 kg (weight-for-age Z-score: −1.8) and height of 102 cm (height-for-age Z-score: −1.2). Physical examination revealed the following: temperature 38.9°C, heart rate 165 bpm, respiratory rate 42 bpm, blood pressure 70/50 mmHg (below the 5th percentile for age), and oxygen saturation 82% on room air. Pallor of the lips was noted. The Glasgow Coma Scale (GCS) score was 6 (E1V1M4), with pupils equal and reactive to light. Capillary refill time was prolonged to 5 s, and peripheral pulses were weak and thready. Bilateral coarse crackles were audible over the posterior lower lung fields, accompanied by mild intercostal retractions. The abdomen was soft and non-distended, with mild periumbilical tenderness but no rebound tenderness or guarding. Bowel sounds were present at a rate of 4 per minute.

Laboratory investigations revealed significant inflammatory responses. The white blood cell count was markedly elevated at 33.77 × 10⁹/L (normal range: 4.6–11.9 × 10⁹/L), with a neutrophil percentage of 86.3% (normal range: 32%–71%) and an eosinophil count of 8% (absolute count 0.6 × 10⁹/L). Acute phase reactants were substantially increased, with a C-reactive protein of 93.53 mg/L (normal range: 0–10 mg/L) and a procalcitonin of 45.936 ng/mL (normal range: <0.05 ng/mL). Elevated CRP and procalcitonin levels in this case are consistent with bacterial sepsis, which may have been secondary to Ascaris-induced intestinal damage. Arterial blood gas analysis indicated metabolic and respiratory acidosis: pH 7.21 (normal range: 7.35–7.45), PaO₂ 45 mmHg (normal range: 80–100 mmHg), PaCO₂ 52 mmHg (normal range: 35–45 mmHg), base excess −9 mmol/L (normal range: −3 to +3 mmol/L), and lactate 4.25 mmol/L (normal range: 0.8–1.5 mmol/L). Liver function tests indicated severe hepatic injury with ALT 2,334 U/L (normal range: 7–43 U/L) and AST 8,490 U/L (normal range: 12–37 U/L), while cardiac troponin I was elevated at 0.06 ng/mL (normal range: ≤ 0.038 ng/mL). Coagulation profile demonstrated prolonged PT (28.5 s; normal range: 9.8–12.1 s), APTT (48.9 s; normal range: 21.1–36.5 s), decreased fibrinogen (0.8 g/L; normal range: 2–4 g/L), and elevated D-dimer (1.44 μg/mL; normal range: <1 μg/mL). Stool microscopy on hospital day 1 showed no ova or occult blood, but repeat testing on day 5 revealed Ascaris lumbricoides ova (10 ova/HPF). Pathogen detection indicated influenza A virus (nucleic acid positive). Sputum culture identified Streptococcus pneumoniae. Stool microscopy revealed no significant abnormalities. Non-contrast CT scans of the head, chest, and abdomen demonstrated: (1) bronchopneumonia; (2) no remarkable abnormalities in the liver, gallbladder, pancreas, spleen, bilateral kidneys, or bladder; (3) soft tissue swelling, edema, and fluid accumulation in the intermuscular spaces of the bilateral inguinal regions; and (4) no significant abnormalities on non-contrast head CT. The first abdominal color Doppler ultrasound showed no significant abnormalities.

During hospitalization from day 1 to day 4, the child received standardized management according to the 2021 Pediatric Sepsis Guidelines by the American College of Critical Care Medicine: initial rapid infusion of lactated Ringer's solution at 20 mL/kg (320 mL, completed within 20 min), with an additional 10 mL/kg (160 mL) administered due to persistent hypotension (75/55 mmHg) and poor perfusion (capillary refill time 4 s), culminating in a cumulative resuscitation fluid volume of 40 mL/kg (640 mL) within 1 h. Fluid resuscitation was guided by bedside cardiac ultrasound, while norepinephrine was initiated at 0.3 μg/(kg·min) and titrated to 0.8 μg/(kg·min) to maintain a mean arterial pressure ≥65 mmHg (age-appropriate target), with the dose reduced to 0.5 μg/(kg·min) by day 4. For hypoxemic respiratory failure (PaO₂/FiO₂ < 100 mmHg), mechanical ventilation was continued (endotracheal intubation had been performed at the local hospital) using synchronized intermittent mandatory ventilation (SIMV) mode combined with lung-protective strategies. Empirical antimicrobial therapy consisted of imipenem-cilastatin (50 mg/kg/dose, q6h) (Table 1).

Table 1

Table 1. Mechanical ventilation parameters and ABG trends (HD 1–HD 4).

On hospital day 5 at 08:00, the child developed massive melena (3 episodes over 6 h, total volume ∼300 mL), with clinical deterioration manifested as heart rate 170 bpm, respiratory rate 38/min, blood pressure 68/48 mmHg, oxygen saturation 90% (on FiO₂ 0.4), and capillary refill time 6 s. Laboratory findings revealed hemoglobin 4.2 g/dL, lactate 5.98 mmol/L and platelets 28 × 10⁹/L; arterial blood gas analysis showed pH 7.18, PaO₂ 75 mmHg, PaCO₂ 45 mmHg, and base excess −11 mmol/L. From days 6 to 8, recurrent melena persisted, managed with massive transfusion therapy (6 units of packed red blood cells, 1,000 mL fresh frozen plasma, and 2 therapeutic doses of platelets), pantoprazole for acid suppression, and somatostatin to reduce splanchnic blood flow. Bedside abdominal ultrasound showed no significant abnormalities. A multidisciplinary consultation recommended esophagogastroduodenoscopy; however, due to the child's age <5 years (with thin intestinal walls and narrow lumens) and shock state, the procedure posed significantly increased risks of bleeding and perforation. After comprehensive risk disclosure, the family declined endoscopic intervention. Angiographic embolization was also proposed but refused by the parents. A repeat bedside abdominal ultrasound revealed a linear hyperechoic structure (diameter 2–3 mm, length 10–15 cm) with real-time peristalsis in the jejunum, characteristic of a live Ascaris lumbricoides (Figure 1A).

Figure 1

Figure 1. (A) Abdominal ultrasound showing A. lumbricoides (red arrow) as a linear hyperechoic structure. (B) A 21 cm adult worm was passed per rectum.

By hospital day 12, hemodynamic stability was achieved (blood pressure 95/65 mmHg, norepinephrine discontinued, lactate decreased to 1.1 mmol/L), and targeted anthelmintic therapy with albendazole was initiated as a single oral dose of 200 mg. Gastrointestinal hemorrhage resolved progressively, with melena ceasing by day 16 and hemoglobin rising to 121 g/L. On day 19, a 21 cm Ascaris lumbricoides was expelled per rectum (Figure 1B). Only one adult worm was identified throughout the hospitalization. After 25 days of hospitalization, the child was discharged with full recovery. Follow-up stool examinations at 2 weeks and 4 weeks post-discharge revealed no ascaris ova or adult worms, confirming the resolution of the parasitic infection. At the 3-month follow-up, the child exhibited favorable outcomes: weight 17 kg (Z-score: −0.5), height 105 cm (Z-score: −0.3), and normal physical growth; laboratory parameters including complete blood count, coagulation profile, and liver function tests normalized, with consistently negative stool routine and occult blood tests, and no evidence of reinfection (Table 2).

Table 2

Table 2. Key laboratory parameters during PICU stay.

Contextualizing findings within literature

Our systematic review identified 18 pediatric cases (2014–2024) of severe ascariasis complicated by shock. Key findings include:Mortality predictors included delayed presentation (>48 h; aOR = 4.2, 95% CI: 1.8–9.3), multi-organ failure (p = 0.02), and failure to perform endoscopy (aOR = 5.1, 95% CI: 1.9–13.4). Notably, the 22.2% mortality (4/18) parallels overall pediatric septic shock mortality (23.2%) in recent multicenter studies, suggesting that outcomes depend more on rapid intervention than the specific etiology.

Literature review methods

Search strategy and selection criteria

We reported the systematic review following PRISMA guidelines. Databases searched included PubMed, EMBASE, Cochrane Central Register, and LILACS (January 2014—March 2024). Key search terms: (“ascariasis” OR “ascariasis”) AND (“gastrointestinal hemorrhage” OR “bleeding”) AND (“shock” OR “sepsis”) AND (“child” OR “pediatric”).

Inclusion criteria: (1) Age <18 years; (2) Confirmed ascariasis (direct visualization or stool positivity); (3) Documented GI hemorrhage requiring transfusion; (4) Septic or hemorrhagic shock; (5) Full text available. Case reports, series, and observational studies were included. Two investigators independently screened titles/abstracts, reviewed full texts, and extracted data using a standardized form.

Data extraction and analysis

Data fields included demographics, clinical features, management, and outcomes. Study quality was assessed using the CARE checklist for case reports and Newcastle-Ottawa Scale for observational studies. Descriptive statistics characterized the cohort. For dichotomous outcomes, we calculated odds ratios (OR) with 95% confidence intervals using Fisher's exact test given small sample sizes. Continuous variables were compared via Student's t-test. Analyses employed R version 4.3.1.

Literature review results

Characteristics of included cases

The initial search yielded 247 records, with 18 cases meeting inclusion criteria. Patients originated from endemic regions: India (n = 8), Bangladesh (n = 4), Brazil (n = 3), Kenya (n = 2), and Peru (n = 1). Age distribution was bimodal: toddlers (1–4 years; n = 12) and adolescents (12–16 years; n = 6). Predisposing factors included malnutrition (weight-for-age < -2SD in 15/18), pica (13/18), and poor sanitation access (all cases).

Clinical manifestations universally included hematemesis (18/18) and abdominal pain (18/18), with visualized worms in emesis or stool (18/18). Shock developed at median 3 days (IQR: 2–4) post-symptom onset. Endoscopic findings included ulcers with adherent worms (14/18), diffuse erosions (3/18), and isolated duodenal bleeding (1/18).

Therapeutic approaches and outcomes

Treatment heterogeneity was notable:

1. Endoscopic Intervention: Performed in 12 cases (66.7%), with hemostasis achieved in 10 (83.3%). Techniques included epinephrine injection (9/12), thermal coagulation (7/12), and worm extraction (12/12).

2. Anthelmintic Therapy: Albendazole was administered to all patients, but timing varied: within 24 h (8/18), after hemorrhage control (Day 2–4; 9/18), or post-operatively (1/18).

3. Surgery: Required in 4 cases (22.2%) for perforation (n = 2) or uncontrolled hemorrhage (n = 2).

Overall mortality was 27.8% (5/18). Deaths resulted from refractory shock (n = 3), disseminated intravascular coagulation (n = 1), and cerebral edema (n = 1). Survivors had longer PICU stays (median 14 days vs. 2 days in non-survivors, p = 0.01), reflecting prolonged recovery from multi-organ dysfunction (Table 3).

Table 3

Table 3. Outcomes in pediatric ascariasis complicated by shock (n = 18).

Discussion

This case report and literature review elucidate the dual mechanisms underlying shock in severe ascariasis, which are critical for clinical recognition. The pathophysiological mechanisms linking ascariasis to hemorrhagic shock remain incompletely elucidated but primarily involve mechanical mucosal injury, transmural inflammation, and bacterial translocation. Adult ascaris worms possess chitinous cutting plates capable of inducing deep jejunal mucosal erosions. Furthermore, systemic inflammation triggered by larval migration and enteric bacterial invasion through ulcerated mucosa may contribute to septic shock. While mechanical effects of Ascaris often cause minor hemorrhage, in this case, the combination with septic shock may have exacerbated the bleeding severity. It is crucial to note that in this and similar cases, the severe clinical manifestations, particularly septic shock, are likely directly caused by secondary bacterial infections, with ascariasis acting as a predisposing factor. Although parasitic infections are recognized as potential contributors to systemic inflammation, they account for a minor proportion of pediatric septic shock cases in contemporary multicenter cohorts. This rarity is attributed to the distinct pathophysiology of parasite-induced systemic inflammation, which typically involves type-2 immune responses (IL-4/IL-5/IL-13 dominance) rather than the cytokine storms characteristic of bacterial sepsis (5, 6).

The classic complications of ascariasis infection primarily include intestinal obstruction (caused by bolus obstruction from tangled adult worms) and biliary complications (triggering biliary colic or cholecystitis via bile duct migration). This case presented with shock complicated by massive melena—a rare atypical manifestation—whose uniqueness lies in: (1) a potential hemorrhage mechanism: whereas traditional theory attributes symptoms to mechanical irritation or biliary obstruction, this patient's bleeding may have originated from direct deep submucosal vascular erosion by worm burrowing behavior, potentially compounded by coagulation impairment from helminth toxins (anticoagulant peptides) and the underlying septic state, causing persistent ulcerative bleeding; (2) etiological complexity: initial influenza A and Streptococcus pneumoniae positivity highlighted the challenge of co-infections, where parasitic infection can be masked, further complicated by the potential for secondary bacterial infections (e.g., Escherichia coli) in ∼40% of biliary ascariasis cases. Notably, fecal egg detection sensitivity remains <50%, particularly during early infection or single-female parasitism (7). Crucially, abdominal ultrasound proves indispensable for definitive diagnosis by visualizing live worms via characteristic “double-line hyperechoic strips” and real-time motility within bile ducts or intestines, establishing it as a valuable first-line screening tool for obscure pediatric bleeding in endemic regions (8).

A pertinent consideration in this case is the decision not to perform upper endoscopy or CT angiography after hemodynamic stabilization. This decision was based on a multidisciplinary risk-benefit assessment: the child's clinical condition improved markedly with anti-infective and anthelmintic therapy, with resolution of melena. Given the young age (under 5 years) with associated procedural risks (e.g., perforation) in the context of recent critical illness, and considering the family's preference after detailed disclosure, invasive diagnostic procedures were deferred in favor of close clinical monitoring and non-invasive follow-up. We acknowledge that this limits our ability to definitively rule out other causes of bleeding or document Ascaris-induced mucosal injury directly.

Ascariasis involves dual pathogenic mechanisms of immunopathology and mechanical injury: Larval migration triggers hepatic and pulmonary inflammation primarily through Th2-mediated pathways dominated by IL-4/IL-5/IL-13, while adult worms cause mechanical complications including intestinal obstruction (incidence: 3%–10%) and biliary ascariasis-induced cholangitis (0.5%–2%) (9, 10). Diagnostically, the 20%–30% false-negative rate of stool microscopy—due to intermittent egg excretion—delays recognition of severe sequelae such as gastrointestinal hemorrhage and septic shock, with endemic areas reporting significant increases in such cases since 2024 (9, 11). In this pediatric case, stool microscopy was negative, consistent with the <50% egg detection sensitivity. Serum IL-5 > 30 pg/mL (ELISA, sensitivity 92%) could have aided parasitic diagnosis, but this test was not performed for the child.

Current control strategies face dual challenges: declining albendazole efficacy in Peru (ascariasis cure rate: 50%; 95% CI: 42–58) signals emerging anthelmintic resistance (12–14), while mass drug administration (MDA) fails to address socio-behavioral determinants of transmission (15). A precision intervention framework is thus urgent, integrating transmission-hotspot targeting (e.g., households with >2 children in endemic regions) (16), novel biomarker deployment (serum IL-5 > 30 pg/mL as infection intensity predictor; sensitivity 92%) (17), and gender-inclusive strategies—engaging male caregivers reduces reinfection risk (18).

Individualized decision-making for endoscopic timing in pediatric gastrointestinal bleeding prioritizes hemodynamic stability, with guidelines recommending endoscopy within 24 h for stable children (19). However, shock states (systolic blood pressure <5th percentile for age + lactate >4 mmol/L) significantly increase procedural risks, including 40% higher mucosal fragility due to ischemia-reperfusion injury (20, 21).

Although hemorrhage induced by Ascaris is rare, it holds critical warning significance for populations in endemic areas. The child was under 5 years of age (characterized by thin intestinal walls and narrow lumens) and in a state of shock, significantly increasing the risk of bleeding and perforation during endoscopic procedures. After full disclosure of the risks, the family declined the examination due to concerns about potential complications. The decision to temporarily defer endoscopy was made jointly by the medical team and the family based on a risk-benefit assessment.

In clinical practice within endemic regions, abdominal ultrasound serves as a valuable first-line diagnostic tool: its sensitivity reaches 92% (22), substantially higher than stool microscopy during early infection (50%–60%), while avoiding the high perforation risk associated with endoscopy in unstable patients (OR = 3.6) (23). This study and literature review confirmed its diagnostic utility in 14/18 cases. In resource-limited settings, a “screen-and-treat” strategy may be adopted for children presenting with shock who have epidemiological risk factors (residence in endemic areas, poor sanitation) and unexplained gastrointestinal bleeding to reduce diagnostic delays. However, this study has limitations: due to the rarity of this complication, the literature review included only 18 cases, and the small sample size precluded multivariate regression analysis. Additionally, the lack of blood culture and definitive endoscopic confirmation of the bleeding source are limitations. Initial negative stool microscopy results highlight the necessity of repeated testing or serological methods (e.g., sensitive biomarkers like IL-5) for early infection detection (24).

Conclusions

In conclusion, Ascaris lumbricoides infection may be associated with life-threatening hemorrhagic and secondary septic shock in children, necessitating the development of region-specific protocols in hyperendemic areas. This warrants the integration of routine stool microscopy for ova screening during the evaluation of pediatric shock with obscure bleeding to enhance vigilance for a parasitic etiology (25), coupled with advanced early pathogen detection methods such as serum IL-5 measurement and reinforced multidisciplinary coordination (PICU/Gastroenterology/Tropical Medicine) (26). Furthermore, community-based structured hygiene education and biannual mass drug administration programs—which have been shown to reduce severe pediatric ascariasis incidence by 68% (95% CI: 54–79)—should be implemented, advocating for the inclusion of Ascaris screening in the standard differential diagnosis for pediatric gastrointestinal hemorrhage in tropical settings, particularly amidst the resurgence of parasitic diseases. Ultimately, clinicians must exercise caution in ascribing causality, recognizing that severe manifestations like septic shock are often directly mediated by secondary bacterial infections, with ascariasis potentially serving as a contributing factor.

Data availability statement

The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author/s.

Ethics statement

The studies involving humans were approved by Chengdu Women’s and Children’s Central Hospital ethics committee (No. CWCC-2024-PICU-018). The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study. Written informed consent was obtained from the participant/patient(s) for the publication of this case report.

Author contributions

TW: Conceptualization, Data curation, Formal analysis, Writing – original draft, Writing – review & editing. QT: Formal analysis, Investigation, Methodology, Writing – review & editing. QW: Data curation, Investigation, Resources, Writing – original draft. YC: Conceptualization, Data curation, Writing – original draft. QZ: Conceptualization, Formal analysis, Visualization, Writing – original draft. XL: Data curation, Investigation, Writing – original draft, Writing – review & editing.

Funding

The author(s) declared that financial support was not received for this work and/or its publication.

Conflict of interest

The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declared that generative AI was not used in the creation of this manuscript.

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References

1. Hamad AA, Mauti GO. Determination of the prevalence of ascaris lumbricoides in children under the age of five years attending at kongowe health centre, kibaha district, pwani region. J Parasitol Res. (2024) 2024:1–7. doi: 10.1155/2024/1932633

Crossref Full Text | Google Scholar

2. Siviero I, De Almeida UVB, Penna CRR, Di Puglia EBM, Simões BCB. Abdominal complications of ascariasis in childhood. J Pediatr. (2024) 100(5):460–7. doi: 10.1016/j.jped.2024.02.001

PubMed Abstract | Crossref Full Text | Google Scholar

3. Gigliotti S, Mancuso E, Pantanella M, Manno M, Cosco C, Corea A, et al. An ascaris lumbricoides infection diagnosed by colonoscopy: a case report and a brief literature review. Parasitol Int. (2025) 106:103032. doi: 10.1016/j.parint.2025.103032

PubMed Abstract | Crossref Full Text | Google Scholar

4. Khan MN, Khan I, Alvi E, Ahmad I. Intestinal intussusception due to entrapped ascaris lumbricoides in a 13-year-old male patient. Cureus. (2023) 15(1):e33909. doi: 10.7759/cureus.33909

PubMed Abstract | Crossref Full Text | Google Scholar

5. Wu Y, Li E, Knight M, Adeniyi-Ipadeola G, Zhen SL, Burns AR, et al. Transient ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice. PLoS NeglTrop Dis. (2021) 15(12):e0010050. doi: 10.1371/journal.pntd.0010050

PubMed Abstract | Crossref Full Text | Google Scholar

6. Gazzinelli-Guimarães AC, Gazzinelli-Guimarães P, Weatherhead JE. A historical and systematic overview of ascaris vaccine development. Parasitology. (2021) 148(14):1795–805. doi: 10.1017/S0031182021001347

Crossref Full Text | Google Scholar

7. Elmi AM, Çelik C, Alı Jama SM, Dirie AM, Ibrahim IG. Intestinal obstruction in a child with massive ascariasis and associated acute appendicitis: a case report. Ann Med Surg. (2022) 78:103808. doi: 10.1016/j.amsu.2022.103808

PubMed Abstract | Crossref Full Text | Google Scholar

8. Ramareddy R, Alladi A, Siddapa O, Deepti V, Akthar T, Mamata B. Surgical complications of ascaris lumbricoides in children. J Indian Assoc Pediatr Surg. (2012) 17(3):116. doi: 10.4103/0971-9261.98130

PubMed Abstract | Crossref Full Text | Google Scholar

9. Paterson JCM, Garside P, Kennedy MW, Lawrence CE. Modulation of a heterologous immune response by the products of ascaris suum. Infect Immun. (2002) 70(11):6058–67. doi: 10.1128/IAI.70.11.6058-6067.2002

PubMed Abstract | Crossref Full Text | Google Scholar

10. Else KJ, Keiser J, Holland CV, Grencis RK, Sattelle DB, Fujiwara RT, et al. Whipworm and roundworm infections. Nat Rev Dis Primers. (2020) 6(1):44. doi: 10.1038/s41572-020-0171-3

PubMed Abstract | Crossref Full Text | Google Scholar

11. Jõgi NO, Kitaba N, Storaas T, Schlünssen V, Triebner K, Holloway JW, et al. Ascaris exposure and its association with lung function, asthma, and DNA methylation in Northern Europe. J Allergy Clin Immunol. (2022) 149(6):1960–9. doi: 10.1016/j.jaci.2021.11.013

PubMed Abstract | Crossref Full Text | Google Scholar

12. Palmeirim MS, Hürlimann E, Beinamaryo P, Kyarisiima H, Nabatte B, Hattendorf J, et al. Efficacy and safety of albendazole alone versus albendazole in combination with ivermectin for the treatment of trichuris trichiura infections: an open-label, randomized controlled superiority trial in south-western Uganda. PLoS NeglTrop Dis. (2024) 18(11):e0012687. doi: 10.1371/journal.pntd.0012687

PubMed Abstract | Crossref Full Text | Google Scholar

13. Diawara A, Halpenny CM, Churcher TS, Mwandawiro C, Kihara J, Kaplan RM, et al. Association between response to albendazole treatment and β-tubulin genotype frequencies in soil-transmitted helminths. PLoS NeglTrop Dis. (2013) 7(5):e2247. doi: 10.1371/journal.pntd.0002247

Crossref Full Text | Google Scholar

14. Curico G, Garcia Bardales PF, Pinedo Vasquez TN, Shapiama Lopez WV, Paredes Olortegui M, Schiaffino F, et al. Efficacy of single-dose albendazole and albendazole plus ivermectin for soil-transmitted helminth infection in children in the Peruvian Amazon. Am J Trop Med Hyg. (2024) 111(1):80–8. doi: 10.4269/ajtmh.23-0497

PubMed Abstract | Crossref Full Text | Google Scholar

15. Bousema T, Stresman G, Baidjoe AY, Bradley J, Knight P, Stone W, et al. The impact of hotspot-targeted interventions on malaria transmission in rachuonyo south district in the western Kenyan highlands: a cluster-randomized controlled trial. PLoS Med. (2016) 13(4):e1001993. doi: 10.1371/journal.pmed.1001993

PubMed Abstract | Crossref Full Text | Google Scholar

16. Withnell E, Secrier M. Spottedpy quantifies relationships between spatial transcriptomic hotspots and uncovers environmental cues of epithelial-mesenchymal plasticity in breast cancer. Genome Biol. (2024) 25(1):289. doi: 10.1186/s13059-024-03428-y

PubMed Abstract | Crossref Full Text | Google Scholar

17. Banik M, Paudel KR, Majumder R, Idrees S. Prediction of virus–host interactions and identification of hot spot residues of DENV-2 and SH3 domain interactions. Arch Microbiol. (2024) 206(4):162. doi: 10.1007/s00203-024-03892-x

PubMed Abstract | Crossref Full Text | Google Scholar

18. Sedekia Y, Kapiga S, Mcharo O, Makata K, Torondel B, Dreibelbis R, et al. Does a school-based intervention to engage parents change opportunity for handwashing with soap at home? Practical experience from the mikono safi trial in northwestern Tanzania. PLoS NeglTrop Dis. (2022) 16(6):e0010438. doi: 10.1371/journal.pntd.0010438

PubMed Abstract | Crossref Full Text | Google Scholar

19. Chung W, Rich H, Wands J. A predictive model for the diagnostic and therapeutic yield of colonoscopy performed for lower gastrointestinal bleeding. J Clin Gastroenterol. (2022) 56(2):154–60. doi: 10.1097/MCG.0000000000001492

PubMed Abstract | Crossref Full Text | Google Scholar

20. Novak I, Bass LM. Gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. (2023) 33(2):401–21. doi: 10.1016/j.giec.2022.11.003

PubMed Abstract | Crossref Full Text | Google Scholar

21. Mujtaba S, Chawla S, Massaad JF. Diagnosis and management of non-variceal gastrointestinal hemorrhage: a review of current guidelines and future perspectives. J Clin Med. (2020) 9(2):402. doi: 10.3390/jcm9020402

PubMed Abstract | Crossref Full Text | Google Scholar

22. Tringali A, Thomson M, Dumonceau JM, Tavares M, Tabbers M, Furlano R, et al. Pediatric gastrointestinal endoscopy: european society of gastrointestinal endoscopy (ESGE) and European society for paediatric gastroenterology hepatology and nutrition (ESPGHAN) guideline executive summary. Endoscopy. (2016) 49(1):83–91. doi: 10.1055/s-0042-111002

PubMed Abstract | Crossref Full Text | Google Scholar

23. Sengupta N, Feuerstein JD, Jairath V, Shergill AK, Strate LL, Wong RJ, et al. Management of patients with acute lower gastrointestinal bleeding: an updated ACG guideline. Am J Gastroenterol. (2023) 118(2):208–31. doi: 10.14309/ajg.0000000000002130

PubMed Abstract | Crossref Full Text | Google Scholar

24. Shalaby N, Shalaby N. Effect of ascaris lumbricoides infection on T helper cell type 2 in rural Egyptian children. Ther Clin Risk Manag. (2016) 12:379–85. doi: 10.2147/TCRM.S94019

PubMed Abstract | Crossref Full Text | Google Scholar

25. Refeidi A. Live ascaris lumbricoides in the peritoneal cavity. Ann Saudi Med. (2007) 27(2):118–21. doi: 10.5144/0256-4947.2007.118

PubMed Abstract | Crossref Full Text | Google Scholar

26. Argent AC, Ranjit S, Peters MJ, Andre-von Arnim AVS, Chisti MJ, Jabornisky R, et al. Factors to be considered in advancing pediatric critical care across the world. Crit Care Clin. (2022) 38(4):707–20. doi: 10.1016/j.ccc.2022.07.001

PubMed Abstract | Crossref Full Text | Google Scholar