Helminthiasis Diagnosis: A Comprehensive Guide for Healthcare Professionals

Introduction

Helminthiasis, commonly known as worm infections, represents a significant global health concern, particularly in underdeveloped and developing nations, although they are also observed in developed countries. Often remaining undiagnosed, these parasitic infections lead to substantial morbidity and, in some instances, mortality due to complications. This article provides an in-depth review of the diagnostic approaches for helminthiasis and emphasizes the crucial role of an interprofessional healthcare team in the accurate evaluation and management of this condition.

Etiology of Helminthiasis

Helminths, derived from the Greek word for “worm,” encompass a diverse group of parasites that can infect humans. These parasites are broadly categorized into “heirlooms,” those inherited from our African ancestors, and “souvenirs,” acquired through contact with animals during human evolution and agricultural practices. Helminthic infections are among the most prevalent infections worldwide, affecting over a quarter of the global population, approximately 2 billion people. This widespread prevalence makes helminthiasis a major health burden, especially for children in developing countries.

The two primary phyla of helminths are nematodes (roundworms) and platyhelminths (flatworms). Nematodes include soil-transmitted helminths (STHs) and filarial worms responsible for lymphatic filariasis (LF) and onchocerciasis. Platyhelminths are further divided into trematodes (flukes), such as schistosomes, and cestodes (tapeworms), including the pork tapeworm that causes cysticercosis. The key soil-transmitted helminths are roundworm (Ascaris lumbricoides), whipworm (Trichuris trichiura), and hookworms (Ancylostoma duodenale and Necator americanus).

Transmission of STHs occurs primarily through contact with soil contaminated with eggs from A. lumbricoides and T. trichiura. Hookworm larvae, conversely, can directly penetrate human skin. Helminthic diseases are often classified as neglected tropical diseases due to their insidious effects on growth and development and the limited research funding they receive, accounting for less than 1% of global research budgets.

Epidemiology of Helminthiasis

Helminthiasis disproportionately affects vulnerable populations. Intestinal parasite infections are a major cause of morbidity and mortality, particularly among children. Key risk factors include residence in rural areas, low socioeconomic status, inadequate sanitation, limited access to clean water, poor personal hygiene, lack of nail trimming, crowded living conditions, insufficient education, limited healthcare access, and substandard housing.

Despite being more prevalent in developing regions, helminthiasis is also present in developed countries. Studies in the USA indicate a significant burden, with estimates of 1.3 to 2.8 million people with serological evidence of Toxocara species infection, 4 million with soil-transmitted helminths, 41,400 to 169,000 with cysticercosis, and about 8000 with schistosomiasis. A study in Chicago highlighted that approximately 12% of recent immigrants tested positive for pathogenic parasite infections, with Toxocara (6.4%) and S. stercoralis (4%) being the most common.

Globally, there has been a reduction in helminthiasis prevalence between 1990 and 2016. For instance, ascariasis prevalence decreased from 1089.36 million in 1990 to 799.68 million in 2016. Similar declines were observed for trichuriasis, hookworm infection, schistosomiasis, lymphatic filariasis, and onchocerciasis. However, soil-transmitted helminthiasis still affects over 2 billion people worldwide.

Pathophysiology of Helminthiasis

Helminths cause damage through both direct and indirect mechanisms.

Direct Damage: This results from the physical presence and activity of worms, including blockage of internal organs or pressure effects from growing parasites.

Indirect Damage: This arises from the host’s immune response to the helminth.

Helminths, being foreign entities, are inherently antigenic and trigger host immune responses. For example, lymphatic blockage by W. bancrofti and granuloma formation in the liver and bladder due to schistosomiasis are hypersensitivity reactions against these parasites. Strongyloides and Trichinella infections can induce chronic intestinal inflammation, potentially leading to villous atrophy and, in severe cases, protein-losing enteropathy. S. stercoralis can also cause Loeffler syndrome via a type 1 hypersensitivity reaction. Trichuris (whipworm) infection can cause colonic inflammation, resulting in blood loss and rectal prolapse.

The severity of indirect damage depends on the intensity and duration of inflammation. Prolonged inflammation from chronic helminth infections can cause irreversible tissue damage and functional loss. Examples include bile duct hyperplasia from long-term liver fluke infection, fibrosis due to schistosomiasis, and skin atrophy in onchocerciasis.

History and Physical Examination in Helminthiasis Diagnosis

A thorough patient history and physical examination are crucial first steps in Helminthiasis Diagnosis. Patients at higher risk often come from developing countries, particularly rural areas with poor sanitation and hygiene. Preschool and school-aged children are frequently affected. Clinical presentations vary widely, depending on the worm burden. Some individuals may have mild infections, while others can harbor a significant number of worms and experience severe symptoms.

Ascariasis: Patients with adult ascariasis can present with acute abdominal symptoms mimicking conditions like upper gastrointestinal bleeding, acute cholecystitis, acute pancreatitis, biliary colic, acute cholangitis, and hepatic abscess. Symptoms may include anemia, fever, jaundice, and abdominal pain and tenderness. Heavy worm burdens can cause small bowel obstruction, characterized by abdominal distension, tenderness, and increased bowel sounds. Severe complications include volvulus, intussusception, gastric perforation, and peritonitis. Other common symptoms of intestinal ascariasis are vomiting (possibly containing worms), weakness, appetite loss, weight loss, diarrhea, or altered bowel habits. In rare cases, pleuritis or pleural effusion may occur. In children, ascariasis can lead to diminished physical fitness, growth stunting, and cognitive impairment. Eosinophilic pneumonia (Loeffler syndrome), caused by A. lumbricoides, can manifest with urticaria, cough, dyspnea, hemoptysis, and abnormal breath sounds. Intestinal parasitic infections, including ascariasis, can also impair micronutrient absorption, leading to malnutrition and weakened immunity.

Hookworm Infections (A. duodenale and N. americanus): Many individuals with hookworm infections are asymptomatic. Skin penetration by larvae may cause intensely itchy, serpentine, vesicular lesions. Hookworms can also cause eosinophilic pneumonia with cough, respiratory distress, and hemoptysis. Wakana syndrome, associated with perioral infection, presents with pharyngeal irritation, cough, nausea, vomiting, and respiratory distress. Intestinal infection can lead to weakness, fatigue, abdominal pain, tenderness or discomfort, tachycardia, tachypnea, anemia, and edema (due to blood and protein loss). Other symptoms may include joint and sternal pain, headache, and impotence.

Strongyloides stercoralis Infection: Often asymptomatic, S. stercoralis can also cause eosinophilic pneumonia, similar to hookworm and A. lumbricoides infections. Chronic strongyloidiasis may manifest with anorexia, nausea, weakness, abdominal pain, tenderness, and diarrhea. Larva currens, a serpiginous urticaria, particularly on the abdomen, torso, groin, and buttocks, is indicative of chronic infection. Reactive arthritis can occur through immune-mediated mechanisms. Strongyloides hyperinfection syndrome, a severe complication in immunocompromised individuals, can lead to intestinal or pulmonary failure and has a high mortality rate if untreated. Disseminated strongyloidiasis, where parasites spread to various organs, can cause catastrophic symptoms such as meningitis, disseminated intravascular coagulation, shock, and renal failure. Immunosuppressed individuals, including those taking corticosteroids or vincristine, those with hematological malignancies, hypogammaglobinaemia, or human T-cell lymphotropic virus type 1 infection, are at increased risk for disseminated strongyloidiasis.

Trichuris trichiura Infection: Most T. trichiura infections are asymptomatic. Loeffler syndrome is not associated with trichuriasis. Symptomatic individuals may experience weakness and abdominal pain. Iron deficiency anemia, finger clubbing, abdominal tenderness, mucoid diarrhea, rectal bleeding, and rectal prolapse can occur, collectively termed Trichuris dysentery syndrome (TDS). Severe T. trichiura infections in children can lead to growth stunting, mental retardation, and cognitive deficits.

Schistosomiasis: Schistosomiasis can be acute or chronic. Acute schistosomiasis (Katayama syndrome) typically presents with sudden onset of fever, fatigue, malaise, myalgia, rash (often urticarial), wheezing, headache, abdominal pain, and eosinophilia. Hepatomegaly and splenomegaly may also be present.

Chronic schistosomiasis manifestations vary depending on the species and location of infection. Intestinal schistosomiasis may cause intermittent abdominal pain, chronic diarrhea, and rectal bleeding. S. mansoni and S. japonicum infections can lead to hepatosplenic disease with periportal fibrosis, upper abdominal discomfort, palpable nodular hepatomegaly, splenomegaly, and portal hypertension, potentially progressing to ascites and hematemesis from esophageal varices. Chronic schistosomiasis can also cause pulmonary hypertension. Urogenital schistosomiasis presents with haematuria, increased urinary frequency, dysuria, and suprapubic discomfort. Urinary tract fibrosis can lead to obstructive uropathy (hydroureter and hydronephrosis), increasing the risk of bacterial superinfection and renal dysfunction. S. hematobium infection is also linked to squamous-cell carcinoma of the bladder. Female genital schistosomiasis can cause pain, stress incontinence, infertility, and increased abortion risk. In men, urogenital schistosomiasis may present with oligospermia, hematospermia, orchitis, and prostatitis. Non-specific symptoms associated with all Schistosoma species include pruritic rash (‘swimmers itch’), low-grade fever, anemia, and malnutrition affecting childhood development. Ectopic egg deposition can lead to rare but serious complications like spinal cord compression or encephalopathy. Cerebral schistosomiasis can manifest as meningoencephalitis with headache, vomiting, blurred vision, fever, and altered sensorium or Jacksonian epilepsy. Spinal cord involvement can present as acute transverse myelitis or subacute myeloradiculopathy, more common in acute schistosomiasis, causing acute lower limb paraplegia or lumbar and leg pain, muscle weakness, sensory loss, and bladder incontinence.

Lymphatic Filariasis (Elephantiasis): Wuchereria bancrofti infection is often asymptomatic. Symptomatic patients may present with fever, malaise, headache, and chills. Characteristic signs include swelling of limbs (elephantiasis) or scrotum (hydrocele), typically affecting single limbs. Red streaks on the skin of arms and legs and painful lymphatic trunks may be observed. Tropical pulmonary eosinophilia, also caused by filariae, presents with asthma-like symptoms, restrictive lung disease, and high eosinophilia. Genital pain and filarial abscesses can also occur.

Echinococcosis (Hydatid Cyst Disease): Most patients with echinococcosis are asymptomatic until complications arise, often leading to accidental diagnosis. Pain in the right hypochondrium is a common presenting symptom. Cyst rupture leading to infection or anaphylaxis, or fistula formation with biliary tract, intestine, or bronchus can cause symptoms.

Taeniasis: Often asymptomatic, taeniasis can cause abdominal pain and distension in intestinal infections. Neurocysticercosis, caused by Taenia solium, can present with recurrent seizures, paresis, obstructive hydrocephalus, headache, intracranial hypertension, stroke, cognitive decline, and depression.

Diphyllobothriasis: Diphyllobothrium latum infection can affect various organs. Central nervous system involvement may manifest as paresthesia and subacute combined degeneration of the spinal cord due to vitamin B12 deficiency. Long-standing infections can cause gastrointestinal symptoms like diarrhea, constipation, abdominal pain, intestinal obstruction, cholecystitis, cholangitis, and subacute appendicitis. Hematological manifestations include megaloblastic anemia, pancytopenia, pernicious anemia, and eosinophilia. Dyspnea can also occur due to prolonged vitamin B12 deficiency.

Diagnostic Evaluation for Helminthiasis

Accurate helminthiasis diagnosis is crucial for effective patient management. Diagnostic methods vary depending on the suspected helminth species and the clinical presentation.

Ascaris lumbricoides Diagnosis: Diagnosis is typically achieved by identifying eggs, larvae, or adult worms.

Stool Microscopy: Detection of Ascaris eggs in stool samples is a primary diagnostic method.
Pulmonary Ascariasis Diagnosis: In Loeffler syndrome, chest X-rays may show pulmonary infiltrates. Bronchoscopy can reveal bronchitis, and filariform larvae may be found in sputum, bronchoalveolar lavage, or gastric aspirate.
Blood Tests: Acute larval infections are often associated with eosinophilia and elevated IgE levels.
Egg Concentration Techniques: Hospital laboratories commonly use egg concentration techniques. The Kato-Katz technique, a simplified field-friendly test, is used for public health control. More sensitive techniques like McMaster, FLOTAC, and mini-FLOTAC, which concentrate eggs, may also be used.
Ultrasonography: Abdominal ultrasonography is a valuable tool for diagnosing hepatobiliary and pancreatic ascariasis. Duodenoscopy and endoscopic retrograde cholangiopancreatography (ERCP) can also be employed.

Trichuriasis Diagnosis:

Stool Microscopy: Stool microscopy is usually sufficient for diagnosing uncomplicated trichuriasis by detecting Trichuris eggs.
Colonoscopy and Biopsy: In severe cases, colonoscopy can identify trichuriasis, and biopsies may be needed for confirmation.
Iron Deficiency Anemia Evaluation: In Trichuris dysentery syndrome, evaluation for iron-deficiency anemia is essential.

Hookworm Infection Diagnosis:

Stool Microscopy: Similar to ascariasis, stool microscopy is the mainstay for diagnosing intestinal hookworm infections by identifying hookworm eggs.
Capsule Endoscopy: Capsule endoscopy can visualize hookworms in the intestine but is rarely used in routine diagnosis.
Anemia Evaluation: Anemia assessment is crucial in hookworm infections due to blood loss.

Strongyloides stercoralis Diagnosis:

Stool Microscopy: Filariform larvae can be detected in wet mount stool preparations, although multiple samples may be needed due to intermittent larval shedding.
Duodenoscopy with Biopsy: Duodenoscopy with duodenal biopsies can reveal eggs, larvae, and adult worms in the intestinal mucosa.
Imaging Studies: Plain abdominal X-rays, contrast-enhanced CT scans, and MRI can assess gut damage.
Tissue Biopsy: In suspected Strongyloides hyperinfection syndrome, biopsies of targeted tissues like lung, bronchial, or small bowel can identify parasites.
IgE and Eosinophil Levels: IgE levels and eosinophil counts may be elevated or depleted in strongyloidiasis, depending on the stage and immune status.

Schistosomiasis Diagnosis:

Microscopic Ova Examination: The gold standard for schistosomiasis diagnosis is microscopic examination of urine (S. haematobium) or stool for ova. The Kato-Katz technique can quantify infection intensity.
Tissue Biopsy: Eggs can also be identified in tissue biopsies from the rectum, bladder, intestine, or liver.
Serology: Serological tests for egg antigens are standard screening methods.
Nonspecific Findings: Eosinophilia, anemia, and thrombocytopenia (due to splenic sequestration) may be present but are not specific for schistosomiasis.
Katayama Fever Diagnosis: Schistosomiasis tests may be negative during Katayama fever, as it occurs before egg laying begins. Diagnosis at this stage relies on clinical suspicion and exposure history.
Abdominal Ultrasonography: Hepatosplenic schistosomiasis can be diagnosed using abdominal ultrasonography to assess liver and spleen involvement.

Lymphatic Filariasis Diagnosis:

Exposure History: History of residence in or travel to endemic areas is a crucial initial step.
Blood Smear for Microfilariae: Microscopic examination of blood smears, ideally collected at night when microfilariae are more prevalent in peripheral blood, can detect microfilariae.
Skin Biopsy: Skin biopsies are typically used for diagnosing tissue-dwelling nematodes like Onchocerca volvulus, not lymphatic filariasis.
Ultrasonography: In asymptomatic males with microfilaraemia, scrotal ultrasonography can visualize lymphatic abnormalities.
PCR, Lymphoscintigraphy, and Immunochromatographic Tests: PCR, lymphoscintigraphy, and immunochromatographic tests are also available for lymphatic filariasis diagnosis.

Echinococcosis Diagnosis:

Laboratory Abnormalities: Elevated ALT, eosinophilia, and fibrinogen levels may be present. Biliary obstruction can lead to elevated transaminases, bilirubin, and gamma-glutamyl transferase. Cyst rupture may significantly elevate gamma-glutamyl transferase and alkaline phosphatase, accompanied by eosinophilia, though these findings are often absent in intact cysts.
Imaging Modalities: Imaging is the primary diagnostic method. Ultrasonography is the most common initial modality. CT scans, MRI, and MRCP provide detailed cyst characterization and assessment of surrounding structures.

Taeniasis Diagnosis:

Stool Examination: Identification of Taenia eggs or proglottids in stool samples can diagnose intestinal taeniasis.
Serological Tests: Enzyme-linked immunoelectrotransfer blot (EITB) for excretory-secretory antigens and enzyme-linked immunosorbent assays (ELISA) for coproantigen detection can aid in diagnosing intestinal taeniasis.
Neurocysticercosis Diagnosis: CT and MRI of the brain are essential for neurocysticercosis diagnosis, visualizing cysts in the brain parenchyma. ELISA can detect parasitic antigens in serum and anticysticercal antibodies in cerebrospinal fluid. EITB assay is also a useful diagnostic tool.

Diphyllobothriasis Diagnosis:

Clinical Features and Laboratory Workup: Clinical symptoms and laboratory findings like megaloblastic anemia, pancytopenia, and eosinophilia raise suspicion.
Stool Examination: Detection of eggs or proglottids in stool samples confirms the diagnosis.
Molecular Methods: PCR and restriction fragment length polymorphism are available for D. latum diagnosis.

Treatment and Management of Helminthiasis

Effective treatment and management of helminthiasis are essential to reduce morbidity and prevent complications.

General Measures: Proper hygiene practices are fundamental in preventing helminth infections.

Ascariasis Treatment: Several anthelmintic drugs are effective, including albendazole, mebendazole, pyrantel pamoate, levamisole, and ivermectin. Intestinal obstruction due to ascariasis requires intravenous support, anthelmintics, and antibiotics. Laparotomy may be necessary for small bowel obstruction, intussusception, or volvulus. Hepatobiliary ascariasis is primarily treated with medication, but endoscopic or surgical intervention may be needed if conservative management fails.

Pharmacology: (This section from the original article is incomplete and would need to be expanded with specific drug regimens, dosages, and considerations for each type of helminthiasis. In a comprehensive article, this section would detail the pharmacological approaches for each helminth infection, including drug choices, mechanisms of action, potential side effects, and contraindications.)

Differential Diagnosis of Helminthiasis

Helminthiasis can mimic various other conditions, necessitating a broad differential diagnosis. These include:

Nutritional deficiencies
Anemia
Asthma
Cholecystitis
Crohn’s disease
Lymphedema
Lymphogranuloma venereum
Tuberculosis
Loeffler syndrome (eosinophilic pneumonia of other causes)
Chronic obstructive pulmonary disease
Inflammatory bowel diseases
Acute bacterial gastroenteritis
Amoebiasis
Giardiasis
Acute pancreatitis
Biliary colic
Intestinal volvulus
Intussusception
Encephalitis
Meningitis
Idiopathic epilepsy
Biliary obstruction
Biliary cirrhosis
Portal hypertension
Liver abscess
Lung abscess
Hepatic cyst (non-parasitic)
Hypothyroidism
Pernicious anemia
Folic acid deficiency

Prognosis of Helminthiasis

The prognosis for helminthiasis varies depending on the specific helminth, the worm burden, and the presence of complications.

Ascariasis: Prognosis is generally good, but heavy worm burdens can lead to serious complications like intestinal obstruction.
Strongyloidiasis: Uncomplicated strongyloidiasis has a good prognosis, but hyperinfection and disseminated strongyloidiasis carry high mortality rates.
Hookworm Infection: Prognosis is excellent with appropriate anthelmintic treatment, iron supplementation, and dietary support.
Echinococcosis: Prognosis depends on the type and location of hydatid cysts. Cystic echinococcosis prognosis is generally good, especially with complete surgical excision. Alveolar echinococcosis has a poorer prognosis.
Diphyllobothriasis: Prognosis is excellent with treatment.
Lymphatic Filariasis: Rarely fatal, with a generally good prognosis for life, though chronic lymphedema is a significant morbidity.
Schistosomiasis: Prognosis for hepatosplenic schistosomiasis is good if hepatic function is preserved. Prognosis is less favorable in patients with advanced portal hypertension, pulmonary hypertension, or cor pulmonale. Overall prognosis depends on worm burden and the stage of disease.
Taeniasis: Prognosis is excellent with anthelmintic treatment, but neurocysticercosis prognosis depends on the location and number of cysts and neurological involvement.

Complications of Helminthiasis

Untreated or severe helminthiasis can lead to numerous complications, including:

Anemia
Malnutrition
Growth retardation
Developmental retardation
Intestinal obstruction
Gastrointestinal hemorrhage
Cor pulmonale
Portal hypertension
Urinary bladder carcinoma (Schistosoma haematobium)
Neurological complications (seizures, myelopathy in neurocysticercosis and cerebral schistosomiasis)
Primary and secondary infertility
Ectopic pregnancy and tubal pregnancy
Hypogonadism
Systemic cysticercosis
Cholangitis
Cholecystitis
Pancreatitis
Cyst or hydatid cyst rupture
Chronic lymphatic damage (lymphedema, elephantiasis)
Blindness (onchocerciasis)

Consultations for Helminthiasis Management

Effective helminthiasis management often requires a multidisciplinary approach. Consultations may include:

Pediatrician or primary care physician (initial diagnosis and management)
Infectious disease specialist (complex cases, unusual presentations)
Gastroenterologist (intestinal helminthiasis, complications)
Hematologist (anemia, eosinophilia)
Nutritionist (malnutrition management)
Hepatologist (hepatic schistosomiasis, echinococcosis)
Neurologist (neurocysticercosis, cerebral schistosomiasis)
Urologist (urogenital schistosomiasis)
Radiologist (imaging for diagnosis and complications)
Surgeon (surgical interventions for complications like intestinal obstruction or hydatid cysts)
Child psychologists and psychiatrists (for cognitive and behavioral sequelae in children)

Deterrence and Patient Education for Helminthiasis

Preventing helminthiasis relies heavily on public health measures and patient education:

Personal Hygiene: Emphasize handwashing, proper cleaning of fruits and vegetables, and sanitary defecation practices. Discourage soil consumption and walking barefoot outdoors in endemic areas.
Public Health Education: Promote hygiene and improved sanitation to reduce infection risk.
Travel Precautions: Advise travelers to endemic areas to avoid contact with fresh water.
Screening: Recommend serological screening for schistosomiasis for individuals returning from endemic regions, even if asymptomatic. Positive serologies should be followed by urine and stool examinations for species identification.
Food Safety: For taeniasis prevention, promote sanitary disposal of human and pig excreta to prevent water contamination. Educate on thorough cleaning, washing, and proper cooking of raw and water-grown vegetables, as well as thorough cooking of beef, pork, and fish.
Pet Management: Educate pet owners on regulating pets, especially dogs, and avoiding unregulated dogs to prevent echinococcosis.

Enhancing Healthcare Team Outcomes in Helminthiasis

Optimal helminthiasis diagnosis and management require a collaborative interprofessional team approach. This team may include primary care physicians, gastroenterologists, internal medicine specialists, infectious disease specialists, hepatologists, neurologists, urologists, radiologists, nutritionists, pharmacists, and surgeons. Effective communication, shared decision-making, and coordinated care are essential to improve patient outcomes. Pharmacists play a crucial role in patient education regarding medication adherence. Interdisciplinary collaboration is vital for providing comprehensive and effective care for patients with helminthiasis.

References

(The reference list from the original article is included here, maintaining the original formatting and links.)

1.Hotez PJ, Brindley PJ, Bethony JM, King CH, Pearce EJ, Jacobson J. Helminth infections: the great neglected tropical diseases. J Clin Invest. 2008 Apr;118(4):1311-21. [PMC free article: PMC2276811] [PubMed: 18382743]
2.Cox FE. History of human parasitology. Clin Microbiol Rev. 2002 Oct;15(4):595-612. [PMC free article: PMC126866] [PubMed: 12364371]
3.Jourdan PM, Lamberton PHL, Fenwick A, Addiss DG. Soil-transmitted helminth infections. Lancet. 2018 Jan 20;391(10117):252-265. [PubMed: 28882382]
4.Novianty S, Dimyati Y, Pasaribu S, Pasaribu AP. Risk Factors for Soil-Transmitted Helminthiasis in Preschool Children Living in Farmland, North Sumatera, Indonesia. J Trop Med. 2018;2018:6706413. [PMC free article: PMC5904775] [PubMed: 29849666]
5.Samuel F, Demsew A, Alem Y, Hailesilassie Y. Soil transmitted Helminthiasis and associated risk factors among elementary school children in ambo town, western Ethiopia. BMC Public Health. 2017 Oct 10;17(1):791. [PMC free article: PMC5634961] [PubMed: 29017470]
6.Wright JE, Werkman M, Dunn JC, Anderson RM. Current epidemiological evidence for predisposition to high or low intensity human helminth infection: a systematic review. Parasit Vectors. 2018 Jan 31;11(1):65. [PMC free article: PMC5791198] [PubMed: 29382360]
7.Mascarini-Serra L. Prevention of Soil-transmitted Helminth Infection. J Glob Infect Dis. 2011 Apr;3(2):175-82. [PMC free article: PMC3125032] [PubMed: 21731306]
8.Awasthi S, Bundy DA, Savioli L. Helminthic infections. BMJ. 2003 Aug 23;327(7412):431-3. [PMC free article: PMC188497] [PubMed: 12933732]
9.Bóia MN, Carvalho-Costa FA, Sodré FC, Eyer-Silva WA, Lamas CC, Lyra MR, Pinto VL, Cantalice Filho JP, Oliveira AL, Carvalho LM, Gross JB, Sousa AL, Moraes TI, Bermudez-Aza EH, Martins EB, Coura JR. Mass treatment for intestinal helminthiasis control in an Amazonian endemic area in Brazil. Rev Inst Med Trop Sao Paulo. 2006 Jul-Aug;48(4):189-95. [PubMed: 17119673]
10.Khuroo MS, Rather AA, Khuroo NS, Khuroo MS. Hepatobiliary and pancreatic ascariasis. World J Gastroenterol. 2016 Sep 07;22(33):7507-17. [PMC free article: PMC5011666] [PubMed: 27672273]
11.Coltart C, Whitty CJ. Schistosomiasis in non-endemic countries. Clin Med (Lond). 2015 Feb;15(1):67-9. [PMC free article: PMC4954528] [PubMed: 25650202]
12.Khaled H. Schistosomiasis and cancer in egypt: review. J Adv Res. 2013 Sep;4(5):461-6. [PMC free article: PMC4293882] [PubMed: 25685453]
13.Durrani MI, Basit H, Blazar E. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Nov 25, 2023. Diphyllobothriasis (Fish Tapeworm Infection) [PubMed: 31082015]
14.Herrick JA, Nordstrom M, Maloney P, Rodriguez M, Naceanceno K, Gallo G, Mejia R, Hershow R. Parasitic infections represent a significant health threat among recent immigrants in Chicago. Parasitol Res. 2020 Mar;119(3):1139-1148. [PMC free article: PMC7075846] [PubMed: 32008064]
15.Hotez PJ. Human Parasitology and Parasitic Diseases: Heading Towards 2050. Adv Parasitol. 2018;100:29-38. [PubMed: 29753341]
16.Wakelin D. Helminths: Pathogenesis and Defenses. In: Baron S, editor. Medical Microbiology. 4th ed. University of Texas Medical Branch at Galveston; Galveston (TX): 1996. [PubMed: 21413312]
17.Marchese V, Beltrame A, Angheben A, Monteiro GB, Giorli G, Perandin F, Buonfrate D, Bisoffi Z. Schistosomiasis in immigrants, refugees and travellers in an Italian referral centre for tropical diseases. Infect Dis Poverty. 2018 Jun 16;7(1):55. [PMC free article: PMC6004084] [PubMed: 29907162]
18.Wang LJ, Cao Y, Shi HN. Helminth infections and intestinal inflammation. World J Gastroenterol. 2008 Sep 07;14(33):5125-32. [PMC free article: PMC2744001] [PubMed: 18777588]
19.Colley DG, Bustinduy AL, Secor WE, King CH. Human schistosomiasis. Lancet. 2014 Jun 28;383(9936):2253-64. [PMC free article: PMC4672382] [PubMed: 24698483]
20.Elbaz T, Esmat G. Hepatic and intestinal schistosomiasis: review. J Adv Res. 2013 Sep;4(5):445-52. [PMC free article: PMC4293886] [PubMed: 25685451]
21.Gonzales I, Rivera JT, Garcia HH., Cysticercosis Working Group in Peru. Pathogenesis of Taenia solium taeniasis and cysticercosis. Parasite Immunol. 2016 Mar;38(3):136-46. [PubMed: 26824681]
22.Hotez PJ, Brooker S, Bethony JM, Bottazzi ME, Loukas A, Xiao S. Hookworm infection. N Engl J Med. 2004 Aug 19;351(8):799-807. [PubMed: 15317893]
23.Shea-Donohue T, Qin B, Smith A. Parasites, nutrition, immune responses and biology of metabolic tissues. Parasite Immunol. 2017 May;39(5) [PMC free article: PMC5863236] [PubMed: 28235148]
24.Karanam L SK, Basavraj GK, Papireddy CKR. Strongyloides stercoralis Hyper infection Syndrome. Indian J Surg. 2021 Aug;83(Suppl 3):582-586. [PMC free article: PMC7223413] [PubMed: 32419745]
25.Ming DK, Armstrong M, Lowe P, Chiodini PL, Doherty JF, Whitty CJM, McGregor AC. Clinical and Diagnostic Features of 413 Patients Treated for Imported Strongyloidiasis at the Hospital for Tropical Diseases, London. Am J Trop Med Hyg. 2019 Aug;101(2):428-431. [PMC free article: PMC6685552] [PubMed: 31219002]
26.Khuroo MS, Khuroo MS, Khuroo NS. Trichuris dysentery syndrome: a common cause of chronic iron deficiency anemia in adults in an endemic area (with videos). Gastrointest Endosc. 2010 Jan;71(1):200-4. [PubMed: 19879568]
27.Kim JB, Seo KI, Moon W. Trichuris trichiura Infection in North Korean Defector Resulted in Chronic Abdominal Pain and Growth Retardation. Korean J Gastroenterol. 2017 Apr 25;69(4):243-247. [PubMed: 28449427]
28.do Espírito-Santo MCC, Magalhães MR, Mortari N, de Siqueira França FO, de Albuquerque Luna EJ, Gryschek RCB. Clinical-epidemiological and laboratory profiles of severe Schistosomiasis mansoni infections at a university hospital. Clinics (Sao Paulo). 2018 Sep 21;73:e340. [PMC free article: PMC6137612] [PubMed: 30281680]
29.Chandy A, Thakur AS, Singh MP, Manigauha A. A review of neglected tropical diseases: filariasis. Asian Pac J Trop Med. 2011 Jul;4(7):581-6. [PubMed: 21803313]
30.Iboh CI, Okon OE, Opara KN, Asor JE, Etim SE. Lymphatic filariasis among the Yakurr people of Cross River State, Nigeria. Parasit Vectors. 2012 Sep 19;5:203. [PMC free article: PMC3519739] [PubMed: 22992226]
31.Mahalingashetti PB, Subramanian RA, Jayker SS, Vijay A. Lymphatic filariasis: A view at pathological diversity. Trop Parasitol. 2014 Jul;4(2):128-32. [PMC free article: PMC4166800] [PubMed: 25250237]
32.Botezatu C, Mastalier B, Patrascu T. Hepatic hydatid cyst – diagnose and treatment algorithm. J Med Life. 2018 Jul-Sep;11(3):203-209. [PMC free article: PMC6197524] [PubMed: 30364592]
33.Agudelo Higuita NI, Brunetti E, McCloskey C. Cystic Echinococcosis. J Clin Microbiol. 2016 Mar;54(3):518-23. [PMC free article: PMC4767951] [PubMed: 26677245]
34.Garcia HH, O’Neal SE, Noh J, Handali S., Cysticercosis Working Group in Peru. Laboratory Diagnosis of Neurocysticercosis (Taenia solium). J Clin Microbiol. 2018 Sep;56(9) [PMC free article: PMC6113464] [PubMed: 29875195]
35.Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol. 2014 Dec;13(12):1202-15. [PMC free article: PMC6108081] [PubMed: 25453460]
36.Ahn CS, Kim JG, Huh S, Kang I, Kong Y. Advances in Serological Diagnosis of Taenia solium Neurocysticercosis in Korea. Genomics Inform. 2019 Mar;17(1):e7. [PMC free article: PMC6459165] [PubMed: 30929408]
37.Lamberton PH, Jourdan PM. Human Ascariasis: Diagnostics Update. Curr Trop Med Rep. 2015;2(4):189-200. [PMC free article: PMC4630244] [PubMed: 26550552]
38.Das AK. Hepatic and biliary ascariasis. J Glob Infect Dis. 2014 Apr;6(2):65-72. [PMC free article: PMC4049042] [PubMed: 24926166]
39.O’Neal S, Noh J, Wilkins P, Keene W, Lambert W, Anderson J, Compton Luman J, Townes J. Taenia solium Tapeworm Infection, Oregon, 2006-2009. Emerg Infect Dis. 2011 Jun;17(6):1030-6. [PMC free article: PMC3320238] [PubMed: 21749764]
40.Parija SC, Ponnambath DK. Laboratory diagnosis of Taenia asiatica in humans and animals. Trop Parasitol. 2013 Jul;3(2):120-4. [PMC free article: PMC3889088] [PubMed: 24470995]
41.Diniz-Santos DR, Jambeiro J, Mascarenhas RR, Silva LR. Massive Trichuris trichiura infection as a cause of chronic bloody diarrhea in a child. J Trop Pediatr. 2006 Feb;52(1):66-8. [PubMed: 16000342]