[Toxocariasis as a cause of hypereosinophilia].

Toxocariasis is one of the causes of eosinophilia in peripheral blood and provokes eosinophilic infiltration in internal organs. In Israel, the number of cases of toxocariasis is very low, 3 cases annually, according to the records at the Ministry of Health. Many cases of eosinophilia might be misdiagnosed as hypereosinophilia syndrome (HES), if serological testing for Toxocara is not conducted, leading to inappropriate treatment. The test is for specific serum IgG antibody of Toxocara canis antigen measured by enzyme-linked immunosorbent assay (ELISA). The authors present a 4 year old girl with hypereosinophilia of 40,000 cell/microl, without involvement of target organs. The authors found that toxocara was the cause of hypereosinophilia. After appropriate treatment the number of eosinophils decreases, presenting a measurement of the parasite activity.

[Bilharziasis caused by Schistosoma mansoni in a traveler returning from Guinea: failure of serodiagnostic testing]. / Bilharziose à Schistosoma mansoniau retour de Guinée: défaillance du sérodiagnostic.

The purpose of this report is to describe a case of febrile hypereosinophilic syndrome in a traveler three weeks after returning from a sightseeing trip to Guinea. Laboratory testing demonstrated an inflammatory response syndrome and hepatic cytolysis. Parasite serology led to suspicion of toxocariasis that was treated using albendazole. Follow-up tests at two months showed the presence of Schistosoma mansoni eggs in stools despite negative standard serodiagnostic testing (hemagglutination). Secondarily Western blot testing of serum samples at one, two and 14 months after returning from Guinea continued to show only protein bands specific to toxocariasis with no bands specific to bilhariziasis. These findings provide further evidence of the limitations of serological testing for detection of bilharziasis in travelers and the difficulty of diagnosis. Guinea is a high-risk tourist destination. Intestinal and urinary bilharziasis are endemic over three-fourths of country. Travelers planning even short stays in areas where bilharziasis is endemic should be advised on preventive measures.

Evaluation of the prevalence and clinical impact of toxocariasis in patients with eosinophilia of unknown origin.

BACKGROUND/AIMS: Eosinophilia has numerous diverse causes, and in many patients, it is not possible to establish the cause of eosinophilia. Recently, toxocariasis was introduced as one cause of eosinophilia. The aims of this study were to evaluate the prevalence of toxocariasis and the clinical impact of albendazole treatment for toxocariasis in patients suspected of eosinophilia of unknown origin. METHODS: We performed a retrospective chart review. After evaluation of cause of eosinophilia, the patients suspected of eosinophilia of unknown origin performed immunoglobulin G antibody specific assay for the Toxocara canis larval antigen by enzyme-linked immunosorbent assay. RESULTS: This study evaluated 113 patients, 69 patients (61%) were suspected of eosinophilia of unknown origin. Among these 69 patients, the frequency of T. canis infection was very high (45 patients, 65.2%), and albendazole treatment for 45 eosinophilia with toxocariasis was highly effective for a cure of eosinophilia than no albendazole group regardless of steroid (82.3%, p = 0.007). Furthermore, among the nonsteroid treated small group (19 patients), albendazole treatment for eosinophilia were more effective than no albendazole group, too (83.3% vs. 28.6 %, p = 0.045). CONCLUSIONS: The prevalence of toxocariasis was high among patients suspected of eosinophilia of unknown origin; therefore, evaluation for T. canis infection is recommended for patients with eosinophilia of unknown origin. Furthermore, for patients suspected of eosinophilia of unknown origin who have positive results for T. canis, albendazole treatment may be considered a valuable treatment option.

Mansonella perstans causing symptomatic hypereosinophilia in a missionary family.

Mansonella perstans is rarely pathogenic. The rare reports of symptomatic cases, however, include severe complications. Three cases of symptomatic hypereosinophilia with multi-organ involvement are described in a missionary family returning from tropical Africa. Pathogenicity may be related to the induction of hypereosinophilia rather than direct host-parasite interactions.

[Parasitic etiology of blood hypereosinophilia]. / Les étiologies parasitaires d'une hyperéosinophilie sanguine.

Blood hypereosinophilia is a common finding in medical practice requiring further investigations. Parasitic diseases are a major cause of eosinophilia and eosinophilia is mainly due to helminths. The investigation of eosinophilia is a long and complicated process. The etiologic diagnosis of eosinophilia requires a review of the patient's history which may reveal travel out of country, symptoms and rate and evolution of eosinophilia. For subjects originating from a country as Tunisia, suspected parasitosis -if eosinophilia is massif- are toxocariasis, distomiasis and scabies. Anguilluliasis and ankylostomiasis will be suspected if the subject is originating from some hot and wet focus. For subjects who have traveled to tropical country, bilharziasis, anguilluliasis and ankylostomiasis will be suspected. Since filariasis and onchocerciasis are diseases by accumulation, they will be suspected if the stay has been long.

Active schistosomiasis, severe hypereosinophilia and rapid progression of chronic endomyocardial fibrosis.

Endomyocardial fibrosis (EMF) is a neglected restrictive cardiomyopathy of unknown aetiology and unclear natural history, which causes premature deaths in endemic areas. We present the case of a 13-year-old boy from a highly endemic area, presenting with concurrent signs of chronic EMF and severe hypereosinophilia associated with active schistosomal cystitis. We discuss the possible role of this parasitic infection in determining the progression of EMF in endemic areas for both conditions.

Löeffler endomyocarditis: a clinical presentation as right ventricular tumor.

A four-year-old girl presented with an apical mass of the right ventricle, pulmonary embolism and hypereosinophilia, and was shown to be infected with Toxocara canis. Cardiac involvement was represented by endomyocardial fibrosis, mainly at the apex of the right ventricle, mural thrombi and tricuspid regurgitation. Hypereosinophilia appears to be the head point at the basis of multiple organ damage in Löeffler endomyocarditis. The disease mechanism proposed is the eosinophilic production of peroxidases, which are cytotoxic when released in large amounts into the blood flow. Treatment is based on etiologic and corticosteroid therapy (prednisolone 1-2 mg/kg/day); surgical therapy is indicated in the end stages of the pathologic process.

[Hypereosinophilia with myocardial involvement due to toxocariasis. Diagnosis of regional myocardial perfusion abnormalities by pulsed tissue Doppler echocardiography]. / Myokardiale Beteiligung des Eosinophilie-Syndroms bei einer Fadenwurminfektion. Nachweis regionaler Myokardrestriktion mittels Pulswellen-Gewebe-Doppler-Echokardiographie.

CASE REPORT: The case of a 57-year-old woman is reported who was admitted for peripheral hypereosinophilia. DIAGNOSIS: Detailed investigations revealed first of all a hypereosinophilic syndrome with infiltration of bone marrow and lung. The patient suffered more and more from angina pectoris with signs of heart failure. Coronary angiography was therefore carried out which showed normal coronary arteries. With suspicion of myocardial involvement endomyocardial biopsies were performed which revealed the presence of Löfflers endocarditis parietalis fibroplastica. Finally, serological studies for parasites disclosed a positive ELISA test for Toxocara, confirmed later to be rising. CONCLUSION: Myocardial involvement of hypereosinophilia, caused by Toxocara is not described until now. Further diagnostic by means of pulsed wave tissue Doppler echocardiography provided regional differentiation of a restrictive filling pattern which documented the importance of this new diagnostic tool in myocardial illness.

Aetiology of endomyocardial fibrosis (EMF).

On epidemiological basis EMF behaves like a vector transmitted disease. The cardiac pathologies of EMF and HES are identical. In some cases of HES, hypereosinophilia may return to normal, leaving residual heart disease that is exactly like EMF. Most temporary residents from Europe and North America who developed EMF while resident in the endemic areas of Africa had hypereosinophilia that was induced by helminths. In our case studies from the EMF endemic areas of Nigeria, most children with acute idiopathic myocarditis associated with helminth induced hypereosinophilia, developed clinical EMF on follow up. We showed also that the rate of decline in the incidence of hypereosinophilia in EMF cases was significantly related to the duration of symptoms. Our studies and other observations show that EMF, like HES is a multiple system disease with similar organ damage. The morphologic evolution of cardiac damage in EMF appears similar to that reported for HES; with a stage of myocarditis/pericarditis, followed by a stage of cardiac necrosis, a stage of thrombosis and by the chronic fibrotic stage. Also during larval migration, all the helminths associated with EMF induce the same spectrum of damage in the central and peripheral nervous system, in the lungs, kidneys and skin, as are reported for HES. The cardiovascular damage reported for these worms (which include hypersensitivity vasculitis, acute myocarditis/ pericarditis) are also similar to what is reported for HES. Acute endomyocardial necrosis and thrombosis that are similar to what is found in HES, have been documented in Trichinella Spiralis and in filariasis. Increased cerium concentrations have been documented in the endocardium of EMF cases from South India. It remains to be established whether cerium excess, which is known to stimulate collagen synthesis does accelerate the process of endomyocardial fibrosis, following cardiac necrosis (which may have been triggered by helminths and the associated hypereosinophilia).

[Diagnostic and treatment of hypereosinophilia upon return from the tropics: 102 patients]. / Diagnostic et traitement des hypereosinophilies sanguines au retour des tropiques: a propos de 102 patients.

Management of blood eosinophilia in travelers returning from the tropics is controversial. In this prospective study, 102 asymptomatic tropical travelers underwent investigation and treatment for hypereosinophilia. In contrast with direct tests for parasitic infection which were positive in only 15% of cases, immunological tests were suggestive of helminthic infection is 77%. The most common diagnoses were toxocarosis (49%), strongyloidiasis (30%), and filariasis (19%). Anti-parasite treatment was undertaken based on laboratory findings (12 cases) or on presumptive diagnosis using two-agent therapy (ivermectin and praziquantel) in 13 cases or three-agent therapy (ivermectin, praziquantel, flubendazole) in 77 cases. As a result of treatment, eosinophil count returned to normal in 61% of cases and decreased in 30%. These findings suggest that presumptive treatment of blood eosinophilia can be undertaken in tropical travelers using three anti-parasitic drugs: ivermectin (1 x 0.4 mg/kg), flubendazole (2 x 100 mg per day for 3 days), and praziquantel (1 x 40 mg). As a precaution before using ivermectin, tests should be performed to detect loiasis which can lead to adverse reactions.

[Genetic control of hypereosinophilias]. / Le controle genetique des hypereosinophilies.

Polynuclear eosinophils play a major role in host defense against infectious diseases and especially helminthiasis. Onset of hypereosinophilia can be attributed to two mechanisms which can occur separately or in combination. The first mechanism involves enhancement of medullary production and differentiation of eosinophils. The second is prolonged life span of eosinophils. Response to eosinophils depends on various cytokines including IL-5, IL-4, IL-3 and GM-CSF. Since it contains the genes coding for these cytokines, the 5q31-q33 region of chromosome 5 is the focus of study on genetic control of human hypereosinophilia. The goal of these studies is to allow screening of subjects predisposed to helminthic infection and to deregulation of immune responses that may lead to atopy and various types systemic inflammatory diseases.

[Reactive hypereosinophilia in parasitic diseases]. / Hyperéosinophilies réactionnelles des parasitoses.

Hypereosinophilia is often linked to the presence of pluricellular parasites in host tissues. Polynuclear eosinophils are sprung from the bone marrow. After multiplying and maturing, they are thrown into the blood flow and from the blood to the tissues where they are found in immediate contact with the parasite. Eosinophils are major components of the parasitic granuloma. Parasitic diseases are a major cause of hypereosinophilia and eosinophilia is mainly due to helminths. Protozoa do not produce hypereosinophilia, except for toxoplasmosis in which a low and discontinuous eosinophilia may be seen. Subsequently, maggots producing myiasis yield to hypereosinophilia too. In helminthiasis, the action of the eosinophil granulocyte is double. In tissues, it destroys the parasite and plays a regulatory role in mastocytes degranulation. Eosinophils which participate in the inflammatory reaction secrete factors which neutralize mediators liberated by mastocytes, histamine mainly, destroyed by histaminase. In a practical point of view, blood hypereosinophilia is a very useful tool for diagnosis. Eosinophilia reach early a high value, this before the parasitic infection becomes detectable by means of resources other than immunological. The eosinophils rates decreases rapidly as an effect of the anthelmintic drug, this confirming the efficacy and specificity of the prescribed treatment.

An unusual case of hypereosinophilia and abdominal pain: an outbreak of Trichostrongylus imported from New Zealand.

We report an outbreak of severe symptomatic Trichostrongylus spp. in travelers visiting a sheep farm in New Zealand. The unusual source of the outbreak was traced as the use of sheep manure as an organic fertilizer on a salad garden.