Complications associated with Toxocara canis infection are rare. We present a case of a patient with Staphylococcus aureus endocarditis as a complication of an endomyocardial fibrosis caused by T canis. The epidemiological, pathological, and clinical features of this rare complication are described here

Balestra, Gianmarco

Blum, Johannes

Kuenzli, Esther

Labhardt, Niklaus

Weisser, Maja

Zellweger, Michael J.

Open Forum Infectious Diseases

PubMed

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Open Forum Infectious DiseasesB R I E F R E P O R TStaphylococcus aureus Endocarditis asa Complication of Toxocariasis-Associated Endomyocarditis WithFibrosis: A Case ReportEsther Kuenzli,1 Niklaus Labhardt,2 Gianmarco Balestra,3 Maja Weisser,4Michael J. Zellweger,5 and Johannes Blum21Division for Infectious Diseases and Hospital Epidemiology, University Hospital Basel andSwiss Tropical and Public Health Institute, Basel, 2Swiss Tropical and Public Health Institute,Basel, 3Medical Intensive Care Unit, 4Division for Infectious Diseases and HospitalEpidemiology, and 5Department of Cardiology, University Hospital Basel, SwitzerlandComplications associated with Toxocara canis infection are rare.We present a case of a patient with Staphylococcus aureus endo-carditis as a complication of an endomyocardial ﬁbrosis causedby T canis. The epidemiological, pathological, and clinical fea-tures of this rare complication are described here.Keywords. endocarditis; endomyocardial ﬁbrosis; Staphy-lococcus aureus; Toxocara species.CASE REPORTIn March 2013, a 45-year-old male patient presented to a hos-pital in Switzerland with fatigue, generalized joint aches, andloss of appetite. Due to an eosinophilia of >8000/µL (normal,<300/µL), a screening for helminthiasis was done using an in-house enzyme-linked immunosorbent assay. It revealed a posi-tive titer for Toxocara spp of 1.75 optical density ([OD] normal,<0.5 OD). In the transthoracic echocardiography, endocardialﬁbrosis was suspected, leading to the diagnosis of toxocaria-sis-associated endomyocarditis. A computer tomography ofthe chest and abdomen showed a splenomegaly and an in-creased number of normal-sized mediastinal and retroperitone-al lymph nodes. Treatment with albendazole 400 mg twice dailyfor 14 days and prednisone 90 mg once daily for 5 days was pre-scribed. During hospitalization, a right subclavian vein throm-bosis was diagnosed, warranting oral anticoagulation.Three months later, eosinophilia was still 800/µL. A secondtreatment course with albendazole was evaluated. Before itcould be applied, the patient presented with acute fever andgeneral malaise.At admission, he was febrile without apparent focus. Thewhite blood cell count was 4.3 × 109/L (normal, 4–10 × 109/L),and C-reactive protein was 26 mg/L (<10 mg/L). Transesopha-geal echocardiography (TEE) showed a mobile structure in theleft ventricular apex (Figure 1). For a presumed infective endo-carditis, intravenous antibiotic therapy with amoxicillin plusclavulanic acid 2.2 g 6 times/day plus gentamycin 90 mg 3times/day was started. All blood cultures drawn at admissionshowed growth of Staphylococcus aureus, leading to the diagno-sis of staphylococcal endocarditis, most likely facilitated by thetoxocariasis-induced endomyocardial ﬁbrosis because thethrombus was in the apex, not on the valves. Therapy wasadapted to ﬂucloxacillin 2 g 6 times/day plus gentamycin 140mg twice a day according to resistance testing.Within hours of admission, the patient developed septicshock and respiratory failure. Repeated TEE showed a decreasedleft ventricular systolic function and a large left ventricularthrombus, increasing in size despite full anticoagulation. Onday 7, it ﬁlled up the apical 50% of the left ventricle. Parts ofit were highly mobile (Figure 1), causing multiple septic emboli.The eosinophils increased from 73/µL on day 2 to 736/µL onday 8. Because septic shock is usually associated with decreasedeosinophils and simultaneously the titer for Toxocara spp was1.04 OD (see Figure 2), we assumed a persisting Toxocara sppinfection. Because ongoing endocardial inﬂammation would fa-cilitate continuous appositional thrombus growth, a secondtreatment course with albendazole 400 mg 3 times daily for 4Figure 1. Transesophageal echocardiography: left ventricular apical thrombus.Abbreviations: Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.Received 24 March 2016; accepted 11 July 2016.Correspondence: E. Kuenzli, Swiss Tropical and Public Health Institute, Socinstrasse 57, Basel4051, Switzerland (esther.kuenzli@unibas.ch).Open Forum Infectious Diseases®© The Author 2016. Published by Oxford University Press on behalf of the Infectious DiseasesSociety of America. This is an Open Access article distributed under the terms of the CreativeCommons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in anymedium, provided the original work is not altered or transformed in any way, and that the workis properly cited. For commercial re-use, please contact journals.permissions@oup.com.DOI: 10.1093/ofid/ofw145BRIEF REPORT • OFID • 1weeks was started. Antibiotic treatment was continued for atotal of 6 weeks.Echocardiographic follow up 6 weeks after completion of an-tibiotic therapy and 4 weeks after completion of albendazoletherapy showed complete resolution of the thrombus. Tenmonths later, parallel titration for Toxocara spp showed atiter of 0.38 OD. Eosinophils were 300/µL, and left ventricularejection fraction and diastolic function had normalized (Figure 3).DISCUSSIONThe patient showed unusual complications of a Toxocara sppinfection. Toxocariasis is a helminth infection of dogs andcats; however, humans are accidental hosts. Most infected hu-mans are asymptomatic, but fever, hepatosplenomegaly, gastro-intestinal, respiratory, neurological, and ocular symptoms orallergic reactions can occur [1, 2]. Clinically relevant cardiacmanifestations, even though rare in humans, include myocardi-tis, pericarditis, Loefﬂer’s endocarditis, and combinations ofthese [3]. The diagnosis is usually based on clinical symptoms,eosinophilia and serological titers.The clinical entity described in our patient is not only consis-tent with previous case reports [4, 5], but it can be explained bypathophysiological processes associated with toxocariasis [6–9]:as in idiopathic hypereosinophilic syndrome, inﬁltration of themyocardium by eosinophils leads to focal myocyte necrosis.The resulting ﬁbrosis is a risk factor for subsequent thrombosis[6, 10]. In addition, peripheral blood eosinophilia caused by par-asitic infections can cause hypercoagulable states, favoringthrombosis [9, 11]. The patient not only suffered from a rightsubclavian vein thrombosis when toxocariasis was ﬁrst diag-nosed, but he showed a growing apical thrombus despite full an-ticoagulation during the second bout of illness.Figure 2. Serological titer and eosinophil count over time. Abbreviation: OD, optical density.Figure 3. Transthoracic echocardiography (at follow up). Abbreviations: LA, leftatrium; LV, left ventricle; RV, right ventricle.2 • OFID • BRIEF REPORTFurthermore, an association between helminth and staphylo-coccal infections has been described. Different potentially caus-ative mechanisms are discussed in the literature: (1) increasedhistamine and immunoglobulin E levels together with eosino-philia impair neutrophil function [12, 13]; (2) bacteria couldbe trapped in the granulomas around the larvae; and (3) com-mon genetic defects predisposing not only for nematode infec-tions but for staphylococcal infections as well have beenpostulated [8].CONCLUSIONSThe case illustrates the difﬁculty of assessing therapeutic respons-es in infections with no clearly deﬁned clinical and laboratoryendpoints. In these situations, treatment success has to be evalu-ated by indirect parameters such as eosinophilia and course ofserologic titers. Repeated and prolonged treatment may be con-sidered if eosinophilia and/or serology remain elevated.AcknowledgmentsPotential conﬂicts of interest. All authors: No reported conﬂicts. Allauthors have submitted the ICMJE Form for Disclosure of Potential Con-ﬂicts of Interest.References1. Despommier D. Toxocariasis: clinical aspects, epidemiology, medical ecology, andmolecular aspects. Clin Microbiol Rev 2003; 16:265–72.2. Holland C, Smith H, eds. Toxocara: The Enigmatic Parasite. Wallingford, Oxford-shire, UK: CABI Publishing; 2006.3. Kuenzli E, Neumayr A, Chaney M, Blum JA. Toxocariasis-associated cardiac dis-ease - a systematic review of the literature. Acta Tropica 2016; 154:107–20.4. De Cock C, Lemaitre J, Deuvaert FE. Löefﬂer endomyocarditis: a clinical presen-tation as right ventricular tumor. J Heart Valve Dis 1998; 7:668–71.5. Traboulsi R, Boueiz A, Kanj SS. Catastrophic aortic thrombosis due to Toxocarainfection. Scand J Infect Dis 2006; 39:283–5.6. Cookston M, Stober M, Kayes SG. Eosinophilic myocarditis in CBA/J mice infect-ed with Toxocara canis. Am J Pathol 1990; 136:1137–45.7. Schaffer SW, Dimayuga ER, Kayes SG. Development and characterization of amodel of eosinophil-mediated cardiomyopathy in rats infected with Toxocaracanis. Am J Physiol 1992; 262(5 Pt 2):H1428–34.8. Moreira-Silva SF, Leite AL, Brito EF, Pereira FE. Nematode infections are risk fac-tors for staphylococcal infection in children. Mem Inst Oswaldo Cruz 2002;97:395–9.9. Ames PR, Aloj G, Gentile F. Eosinophilia and thrombosis in parasitic diseases: anoverview. Clin Appl Thromb Hemost 2011; 17:33–8.10. Corradi D, Vaglio A, Maestri R, et al. Eosinophilic myocarditis in a patient withidiopathic hypereosinophilic syndrome: insights into mechanisms of myocardialcell death. Hum Pathol 2004; 35:1160–3.11. Rohrbach MS, Wheatley CL, Slifman NR, Gleich GJ. Activation of platelets by eo-sinophil granule proteins. J Exp Med 1990; 172:1271–4.12. Davis SD, Schaller J, Wedgwood RJ. Job’s syndrome. Recurrent, “cold”, staphylo-coccal abscesses. Lancet 1966; 1:1013–5.13. Caldwell K, Lobell M, Coccia PF. Mitogenic response to Toxocara antigen and che-motactic defect in visceral larva migrans. Am J Dis Child 1980; 134:845–7.BRIEF REPORT • OFID • 3

Staphylococcus aureus Endocarditis as a Complication of Toxocariasis-Associated Endomyocarditis With Fibrosis: A Case Report

AbstractComplications associated with Toxocara canis infection are rare. We present a case of a patient with Staphylococcus aureus endocarditis as a complication of an endomyocardial fibrosis caused by T canis. The epidemiological, pathological, and clinical features of this rare complication are described here.</jats:p

Staphylococcus aureus Endocarditis as a Complication of Toxocariasis-Associated Endomyocarditis With Fibrosis: A Case Report

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