Travel-acquired subcutaneous<i>Sparganum proliferum</i>infection diagnosed by molecular methods
Authors: F. Schauer, S. Poppert, K. Technau-Hafsi, M. Mockenhaupt, B. Muntau, G. Häcker, D. Tappe, T. Jakob
Journal: British Journal of Dermatology (2013)

Funding sources: none Conflicts of interest: none declared Dear Editor, Sparganosis is a parasitic zoonosis caused by the plerocercoid, i.e. infective larva (sparganum), of pseudophyllidean tapeworms belonging to the genus Spirometra. Human infections with spargana are classified into two forms: nonproliferative sparganosis and proliferative sparganosis. Nonproliferative sparganosis is endemic mainly in East and Southeast Asia (China, Japan, Korea, Taiwan and Thailand) and is caused by Spirometra erinaceieuropaei (Spirometra mansoni) in the Old World and Spirometra mansonoides in the New World. Proliferative sparganosis is caused by the more pathogenic and disseminating Sparganum proliferum and is only sporadically reported from Asia (Japan, Taiwan, Thailand) and very rarely from the New World (Paraguay, Venezuela, U.S.A.).1 2 We present a case of a 61‐year‐old European man who was admitted to our hospital after a holiday travelling through Bolivia, Brazil and Paraguay. Upon his return to Germany he noticed an itching reddish patch on his right chest. During the following 3 weeks the patch grew constantly in size up to 10 cm in diameter and the central part became darker and tumescent (Fig. 1a). He had no impairment in his general condition. Ultrasound showed a hyperechoic strand‐shaped formation with discrete surrounding oedema in the dermis. Excision of the structure exposed a white cestode‐like helminth of 4 cm length with flattened ends and 2–3 mm body width (Fig. 1b). The helminth was extracted easily from the surrounding tissue. The excision was performed along the macroscopic structure to make sure that the entire organism was removed. There were no signs of muscle infiltration in the depth. Histological examination showed dermal perivascular cuffing with lymphocytes, histiocytes and prominent eosinophils (Fig. 1c). The central part showed a cavity surrounded by necrotic tissue and inflammation. Laboratory investigations revealed a mild eosinophilia of 7·3% (total eosinophil count 0·48 × 109 L−1), and elevated γ‐glutamyltransferase (103 IU L−1) and alanine aminotransferase (69 IU L−1), while the remaining differential white blood cell count, kidney function tests, electrolytes, C‐reactive protein and erythrocyte sedimentation rate were within normal ranges. Chest X‐ray and abdominal ultrasound were normal. Hepatitis B and C, and HIV infection could be excluded. Immunoglobulin levels and peripheral blood lymphocyte subpopulations were normal. The formalin‐fixed, paraffin‐embedded specimen was subjected to polymerase chain reaction amplification followed by sequencing of parasite genes in a reference centre (Bernhard Nocht Institute, Hamburg, Germany). Genes coding for mitochondrial cytochrome C oxidase subunit 1 (primers Cox1F and Cox1R),3 mitochondrial NADH dehydrogenase subunit 3 [primer NADH3‐CES‐F4 (ggtaaatcgtRatgctgtt) and the newly designed primer NADH3‐CES‐R (taccMacacgcttatga)], as well as mitochondrial (mt)12SrRNA (primers 12S‐Taenia FF and 12S‐Taenia‐RR),5 were analysed. The identified nucleotide sequences showed high homology to database entries of S. proliferum (Cox1: 98%; NADH3: 96%; mt12SrRNA: no S. proliferum sequences available) and lower homology to sequences of S. erinaceieuropaei (Cox1: 90%; NADH3: 86%; mt12SrRNA: 92%). The infecting parasite was thus identified as S. proliferum by molecular methods.