IgE-mediated Anisakis allergy in children

Anisakids are nematodes responsible for different clinical patterns in humans. The well-known human-infecting Anisakis species include members of the Anisakis simplex (AS) complex. Humans usually contract anisakiasis through ingestion of raw or undercooked seafood containing Anisakis larvae. Once Anisakis has been ingested, patients may develop disease driven directly by Anisakis larvae and/or by allergic reaction due to this nematode. The capability of inducing allergic reactions depends on the expression of specific antigens by nematodes and host factors. This study aims to resume actual knowledge about AS and Anisakiasis with regard to epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment. Particular attention is paid to Anisakis allergens and their cross-reactivity on available diagnostic methods, and defining a diagnostic pathway for Anisakis allergy. Because only a few data are available in the literature about pediatric population, we focus on this group of patients specifically (AU)

A Case Report of Adhesional Small Bowel Obstruction Caused by Extraintestinal Anisakiasis.

BACKGROUND: Small bowel obstruction (SBO) is a common diagnosis made in the emergency department (ED). We present a case with an unusual underlying cause of SBO: extraintestinal infection with an Anisakis roundworm. CASE REPORT: A healthy young woman with no prior abdominal surgery presented with epigastric abdominal pain, nausea, and anorexia 1 day after eating a raw oyster. Laboratory studies were significant for 14% eosinophilia. Initial abdominal computed tomography (CT) showed small bowel inflammation and small-volume ascites. After discharge home, she returned on day 14 of illness with a closed-loop SBO, to which she was predisposed by an adhesion formed in association with an eosinophilic abscess containing an Anisakis roundworm. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Anisakiasis is an uncommon cause of common symptoms with which patients may present to EDs. The diagnosis should be considered in patients presenting with abdominal pain and recent ingestion of raw seafood, with suspicion raised further by the presence of focal gastric or small bowel inflammation and ascites on abdominal CT. Extraintestinal anisakiasis can cause inflammation leading to intraabdominal adhesions, a sequela of which is small bowel obstruction. If suspicion for gastric or intestinal anisakiasis is high, treatment with endoscopic removal or albendazole may be initiated.

Exploring tumourigenic potential of the parasite Anisakis: a pilot study.

Anisakiasis is a global disease caused by consumption of raw or lightly cooked fish parasitised with Anisakis spp. third-stage larvae. Cases in the literature show colocalised anisakiasis and colorectal cancer, and the incidental finding of Anisakis larvae at the tumour site was reported. Data from our group suggested an epidemiological link between previous infection and gastrointestinal cancer. Furthermore, it has recently been reported that Anisakis products lead to inflammation and DNA damage. Based on these facts, the aim was to investigate whether Anisakis antigens are able to induce changes in the proliferation of epithelial cells in vitro or in the expression of serum microRNA (miRNA) in Sprague-Dawley rats. Anisakis complete extract (CE) induced increases in cell proliferation and decreases in apoptosis compared with nontreated cells, which resulted in a significant increase in the absolute number of viable cells at 48 h of exposure (P < .05). Furthermore, the miRNAs mmu-miR-1b-5p and mmu-miR-10b-5p (a cancer-related miRNA) were significantly decreased (P < .05) in sera from the rats inoculated with Anisakis CE, compared with control rats inoculated with saline. Additionally, based on their relative quantification values, four other cancer-related miRNAs were considered to be differently expressed, rno-miR-218a-5p and mmu-miR-224-5p (decreased) and rno-miR-125a-3p and rno-miR-200c-3p (increased). Anisakis CE was able to induce changes both in epithelial cells in vitro and in an animal model. The results obtained with Anisakis CE, in terms of increasing cell proliferation, decreasing apoptosis and inducing changes in the expression of serum cancer-related miRNAs in rats, suggest that Anisakis could have tumourigenic potential.

Should the host reaction to anisakiasis influence the treatment? Different clinical presentations in two cases / ¿Debe la reacción frente la anisakiasis influir sobre el tratamiento? Presentación clínica

Gastrointestinal anisakiasis is a parasitic infection occurring in people that consume raw or inadequately cooked fish or squid. It is frequently characterized by severe epigastric pain, nausea and vomiting caused by the penetration of the larvae into the gastric wall. Acute gastric anisakiasis with severe chest discomfort is rarely reported in Italy. On the other hand, gastro-allergic anisakiasis with rash, urticaria and isolated angioedema or anaphylaxis is a clinical entity that has been described only recently. Also, if patients usually develop symptoms within 12 hours after raw seafood ingestion, not always endoscopic exploration can promptly identify the Anisakis larvae. Moreover, some authors consider the prevailing allergic reaction as a natural and effective defense against the parasitic attack. We report two cases of peculiar manifestations of anisakiasis in both acute and chronic forms (severe chest discomfort and anaphylactoid reaction)(AU)

Multiple acute parasitization by Anisakis simplex.

Hypersensitivity to Anisakis is an increasingly prominent medical problem throughout the world, due to a better understanding of diseases induced by parasites and to modern culinary habits of eating raw or undercooked fish. We describe the case of a patient who presented epigastric pain, wheals, erythema, and pruritus 3 hours after the ingestion of fish. More than 200 larvae were obtained by endoscopy. However, the patient only developed an immune response with specific immunoglobulin E and eosinophilia peaking at day 18 and decreasing during the 17-month follow-up. Only eosinophilia reached normal limits.

Anisakiasis, an underestimated infection: effect on intestinal permeability of Anisakis simplex-sensitized patients.

Anisakis simplex is a parasite that, if present in uncooked and contaminated saltwater fish, can invade the human gut. Two different clinical situations are recognized: the first, known as a gastrointestinal disease, varying from an asymptomatic episode to vomiting and diarrhea, and the second, classified as an adverse reaction to food, characterized by a wide spectrum of allergic reactions like rhinitis, conjunctivitis, or even anaphylaxis causing hypotension and/or shock. The intestinal epithelium, the major defense system against external molecules, represents an open gate for toxins and allergens if its protective function is compromised. Previous data have demonstrated a strict relationship between an altered intestinal permeability (I.P.) and worsening of the clinical manifestations in patients with adverse reactions to the food. In this article we evaluated the sensitization to A. simplex among patients who referred clinical symptoms of allergy. All subjects underwent commonly used alimentary skin prick test for food allergens, to which Ani s1, an A. simplex allergen, was added. In addition, in A. simplex-sensitized subjects, I.P. was determined upon their enrolment to the study (time 0) and after 6 months of consuming a raw fish-free diet (time 6). Five hundred and forty subjects were screened, and 170 had a positive skin prick test, 87 (51.2%) of whom were positive to Ani s1. Increased I.P. was evidenced in A. simplex-sensitized subjects with worse clinical symptoms, which receded after 6 months' elimination of raw seafood. With our data we demonstrated that the alimentary habit to eat raw fish represents a high risk for the integrity of the intestinal mucosa, and we suggest that this pathological situation may constitute an ideal, under-estimated, open gate for molecules that predispose to other, more important pathologies.

Anisakiasis intestinal diagnosticada por enteroclisis / Intestinal anisakiasis diagnosed by enteroclysis

La anisakiasis es una parasitación frecuente en nuestro medio y que da lugar a cuadros de dolor abdominal que pueden simular otras patologías, incluyendo situaciones quirúrgicas (apendicitis o peritonitis), pero generalmente autolimitadas. Presentamos un caso de una paciente de 48 años con dolor abdominal agudo, febrícula y hallazgos patológicos en TAC (propios de un cuadro inflamatorio intestinal), en la que la realización de una enteroclisis fue capaz de identificar larvas de Anisakis. La paciente evolucionó favorablemente con tratamiento conservador y el patrón radiológico volvió a la normalidad. En nuestro caso, la posibilidad de contar con una técnica radiológica objetiva que sirvió de ayuda al diagnóstico proporcionó datos muy útiles en el manejo de la paciente. Se revisan las características clínicas y radiológicas de la enfermedad (AU)

Anisakiasis is a common infestation in our setting that produces abdominal pain that can simulate other diseases including surgical conditions (symptoms of acute abdomen, mimicking appendicitis or peritonitis), but it is generally a self-limiting process. We report a case of a 48-year-old female with acute abdominal pain, fever and pathological findings on the CT scan (inflammatory bow condition). Anisakis larvae could be identified by the enteroclysis. The patient evolved favorably with conservative treatment and radiologic intestinal pattern returned to normal. The possibility of a radiological technical to assist in the diagnosis provided very useful data in the management of our patient. The radiological and clinical features of the disease are reviewed (AU)

Histopathology and ultrastructure of Platichthys flesus naturally infected with Anisakis simplex s.l. larvae (Nematoda: Anisakidae).

The histopathology, ultrastructure, and immunohistochemistry of the alimentary canal of flounder Platichthys flesus (L.), naturally infected with the nematode Anisakis simplex s.l. (Rudolphi 1809) from the River Forth (Scotland), were investigated and described. Eight of the 16 flounders were infected with A. simplex s.l. larvae (L3); parasites were encapsulated by serosa on the external surface of the host's digestive tract (intensity of infection 1-8 parasites per host), although nematode larvae were found encysted under the peritoneal visceral serosa of the host spleen and liver and, occasionally, in the liver parenchyma (intensity of infection 3-10 parasites per host). In all sites, different structural elements were recognized within the capsule surrounding larvae. Among the epithelial cells of the intestine of 5 flounders with larvae encysted on external surface of the gut, the presence of several rodlet cells (RCs) was observed. Furthermore, often the occurrence of macrophage aggregates (MAs) was noticed in infected liver and spleen, mainly around the parasite larvae. Eight neuropeptide antisera were tested with immunohistochemistry methods on gut sections of 4 P. flesus infected with extraintestinal nematodes. Sections from the gut of 5 uninfected flounder were used for comparative purposes. In the tunica mucosa of parasitized P. flesus, several endocrine epithelial cells were immunoreactive to anti-CCK-39 (cholecystokinin 39) and -NPY (neuropeptide Y) sera; furthermore, in the myenteric plexus, a high number of neurons were immunoreactive to antibombesin, -galanin, and several to -NPY and -PHI (peptide histidine isoleucine) sera.

Freezing infective-stage larvae from Anisakis simplex and their produce at -20 degrees C for 24 h does not prevent the occurrence of autonomic imbalance in rat ileum.

UNLABELLED: In the present report, we analyze the efficacy of the sanitary regulations to kill the Anisakis simplex larvae (As L3) (heat or freeze) to avoid the gastrointestinal alterations that it provokes. We studied the effects on intestinal contractility (muscular tone, amplitude, and frequency of the twitches and cholinergic and alpha-adrenergic stimulus) of As L3, their crude extracts (CE) and excretory-secretory products (ESP), untreated or heated (60 degrees C for 15 min) or frozen (-20 degrees C for 24 h) using rat ileum and an isometric system. Carbachol and noradrenaline have been used as cholinergic and alpha-adrenergic stimulus, respectively. We determined that viable As L3, their untreated CE and ESP, as well as all their frozen counterparts, altered the intestinal contractile activity and its autonomic control. In contrast, heated As L3, CE, and ESP were incapable of provoking any change in rat ileum motility, suggesting an inhibitory effect by the heating procedure. IN CONCLUSION: 1) The gastrointestinal alterations provoked by As are not necessarily associated with a prior infection; and 2) the storage of the seafood at -20 degrees C during 24 h does not prevent the intestinal autonomic imbalance provoked by As, whereas, the prior heating at 60 degrees C for 15 min may completely prevent such process.

Intestinal localization of anisakiasis manifested as acute abdomen.

Anisakis pathology is due mainly to two mechanisms: allergic reactions (from isolated urticaria and angioedema to life-threatening anaphylactic shock associated with gastrointestinal symptoms or 'gastroallergic anisakiasis'), and direct tissue damage, due to invasion of the gut wall, development of eosinophilic granuloma, or perforation (gastric or intestinal anisakiasis). Anisakiasis is a misdiagnosed and underestimated cause of acute abdomen: most patients undergo laparotomy, and virtually no cases are diagnosed before surgery. In some cases, diagnosis is obtained accidentally during other pathologic investigations. We report a case of acute abdomen due to terminal ileum involvement. Microscopic examination of the resected segment showed the presence of helminthic sections consistent with larvae of Anisakis spp. A history of raw fish ingestion was recorded. Histopathologic features are illustrated. A short but up-to-date review of the literature on diagnostic devices (particularly imaging and serology), clinical aspects and therapy is presented.

Altered autonomic control in rat intestine due to both infection with Anisakis simplex and incubation with the parasite's crude extract.

Anisakis simplex IgE may bring on allergic responses such as angioedema, vomiting, and urticaria from eating seafood, but it is not the only etiology. Induced cholinergic hyperreactivity or adrenergic blockade in the target tissue can cause these diseases nonimmunologically also. Here we studied the effects on normal intestinal motility of brief A. simplex infections and in vitro exposures to the parasite's extract (CE). Each approach was evaluated according to its ability to induce cholinergic hyperreactivity or adrenergic blockade in rat duodenum (RD), jejunum (RJ), and ileum (RI) in vitro. Additionally, bolus propulsion in RD, RJ, and RI was evaluated with time in vivo utilizing animals infected 4 h previously with A. simplex larvae (L3) vs sham animals. Tissues, after inoculation of 1, 5, 10, and 20 L3, exhibited time- and dose-dependent motility changes after carbachol (Ch) and noradrenaline (NA), justifying our using herein rats from the fourth hour of infection with 20 L3. We observed a persistent, yet differential effect of the infection on RD, RJ, and RI responses to Ch or NA. It caused cholinergic (muscarinic) hyperreactivity in RD only, and adrenergic blockade in all other parts, and consequently increased the transit index in RD, not in RJ or RI. In contrast, exposing RD, RJ, and RI to CE persistently increased both parameters, amplitude of twitches and muscular tone, in all, albeit that, here also, responses to Ch and NA were CE dose dependent. Interestingly, sensitivity to CE was in the order RI > RJ > RD, the reverse situation of that observed during active infection. Thus, previously viable A. simplex L3, after digestion, can exert bystander disturbance in autonomic control in the whole intestine. Our findings demonstrate that A. simplex L3, alive or dead, can induce cholinergic hyperactivity and adrenergic blockade in the whole small intestine and, as a consequence, gastrointestinal symptoms. Significantly, they may do so long before parasite-specific IgE is detectably induced or despite the occurrence of such IgE.

Propuesta para una clasificación de la alergia a los alimentos / Proposal for a classification of food allergy

Introducción: Aunque parece que el interés por la alergia a los alimentos ha crecido en los últimos años y que cada vez se diagnostican más pacientes adultos, la mayoría de los conceptos se basan en la alergia a los alimentos que se ven en los niños. Se propone una clasificación de la alergia a los alimentos mediada por IgE basada tanto en la capacidad de los alimentos para inducir síntomas, en la susceptibilidad de los sujetos para reaccionar a ellos y en sus posibles variaciones con la edad. Clasificación: 1. Alergia a los alimentos independiente: el alimento es necesario y suficiente por sí mismo para desencadenar una reacción alérgica en los sujetos sensibilizados. 1. 1. Alergia a los ali-mentos primaria: los alergenos son capaces de sensibilizar a sujetos predispuestos (alergenos completos). 1. 1. 1. Alergia a los alimentos de la infancia: "alergia a los alimentos clásica". Probablemente la inmadurez (tanto del aparato digestivo como del sistema inmunitario) favorecen la sensibilización en los primeros contactos con el alimento. 1. 1. 2. Alergia a los alimentos del adulto: pacientes monosensibilizados que comienzan a tener síntomas en la edad adulta. De existir estos pacientes, la patogenia estaría sin aclarar. 1. 2. Alergia a los alimentos secundaria: los alergenos alimentarios responsables no son capaces de sensibilizar a través del aparato digestivo (alergenos incompletos). Los síntomas ocurrirían en pacientes sensibilizados antes por vía respiratoria, cutánea, etc. Incluye el síndrome de la alergia oral, pero también síntomas sistémicos, y podría deberse a la reactividad cruzada existente entre los alergenos. 2. Alergia a los alimentos dependiente: el alimento es necesario pero no suficiente para desencadenar una reacción clínica en los sujetos sensibilizados. Los alergenos alimentarios podrían en este caso estar "excluidos" o ser incapaces de contactar con el sistema inmunitario (alergenos excluidos o protegidos). Sería necesario algún factor adicional para que ocurriera una reacción clínica. La alergia a los alimentos dependiente del ejercicio sería el modelo. También podrían ser importantes otros factores menos estudiados (fármacos, infecciones, etc). 3. Aler-gia relacionada con los alimentos: los alimentos están relacionados con la aparición de los síntomas pero no está claro si son necesarios, importantes o simplemente espectadores. Se trataría de un grupo observacional en el que poder situar temporalmente a los pacientes mientras se encuentra un diagnóstico definitivo. Los sujetos con alergia a Anisakis son un ejemplo de pacientes que debieran haber permanecido en este grupo. 4. Alergia a los alimentos por vía no digestiva: el alimento es capaz de producir síntomas por inhalación o contacto. Incluye tanto la alergia grave a los alimentos como las enfermedades ocupacionales provocadas por los alimentos (asma ocupacional, dermatitis proteínica,etc). Conclusiones: Esta propuesta intenta aumentar nuestra comprensión de la alergia a los alimentos incluyendo para ello a todos los pacientes con síntomas sugestivos de alergia a los alimentos mediada por IgE. También podría ayudar a interpretar algunas de las discordancias que a veces se observan entre la anamnesis y el estudio alergológico. Si la demostración de una relación causa-efecto entre un alimento y los síntomas es fundamental para confirmar el diagnóstico, su ausencia puede no ser suficiente para excluirlo (AU)

Gastroallergic anisakiasis: borderline between food allergy and parasitic disease-clinical and allergologic evaluation of 20 patients with confirmed acute parasitism by Anisakis simplex.

BACKGROUND: Human subjects can be parasitized by Anisakis simplex by eating raw or undercooked fish. Gastric anisakiasis is probably the most frequent clinical entity presenting with severe epigastric pain, vomiting, and diarrhea. In gastroallergic anisakiasis hypersensitivity symptoms predominate. OBJECTIVE: We sought to describe clinical features, laboratory data, and gastroscopic findings in gastroallergic anisakiasis. METHODS: We selected 40 patients presenting to the emergency department with an acute allergic reaction, and if we suspected acute parasitism by A simplex, a fiberoptic gastroscopy was performed. In 20 patients we could detect one or more nematodes; these patients are referred to as group A. Those in whom no worm could be found are referred to as group B (n = 20). A detailed history, clinical features, gastroscopic findings, laboratory data, and skin prick test responses were compared. RESULTS: Long-time intervals of up to 26 hours between fish intake and onset of hypersensitivity symptoms were found (group A, 5.4 +/- 6.3 hours; group B, 5.3 +/- 2.6 hours). Patients in groups A and B did not differ with respect to allergic symptoms (urticaria, angioedema, erythema, bronchospasm, and anaphylaxis) or the mainly light abdominal symptoms (upper abdominal pain, nausea, vomiting, and diarrhea). No significant differences were found with respect to age, time interval between fish intake and onset of symptoms, white cell and eosinophil counts, specific IgE levels against A simplex, or total IgE levels. CONCLUSIONS: The peculiar sometimes long-time interval between fish intake and onset of allergic symptoms render the diagnosis difficult. An early gastroscopy can confirm the diagnosis and prevent complications. We suggest that gastroallergic anisakiasis be considered a distinct clinical entity in which the predominant symptoms are hypersensitivity symptoms and in which the correct diagnosis is not only important in the management of the acute reaction but also in the prevention of further allergic episodes.