Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 19, Number 9—September 2013

Alaria alata Infection in European Mink

Cite This Article

To the Editor. Alariosis is a reemerging zoonotic disease caused by infection with larval stages of trematodes of the genus Alaria. The trematodes are found in wildlife that inhabit wetlands, and these animals may serve as possible reservoirs for these organisms that cause human infection (1). The main sources for human infection are suids and frogs (1). In humans, the clinical features of alariosis caused by infections with the North American species of Alaria vary from mild and asymptomatic to moderate with respiratory or cutaneous signs (2) or neuroretinitis (3), to severe-to-lethal anaphylactic shock caused by larva migrans (4,5). The genus Alaria has 7 species; only A. alata is found naturally in Europe (6), a species which has not thus far been shown to be responsible for human infections.

A. alata infection is common in its typical definitive host (red fox, Vulpes vulpes) and in certain paratenic hosts (wild boar, Sus scrofa) (1). However, the role of other paratenic hosts is poorly known. Among these, mustelids are reported to harbor mesocercariae of A. alata trematodes (7). The pathogenic effect of A. alata infection has been poorly studied, because most lesions described were in humans infected with other species of Alaria. Except for 2 experimental studies that described gross lesions produced by A. alata trematodes (6,8), to our knowledge, no data have been published concerning lesions produced by natural infection in nonhuman hosts. Our report provides a detailed description of the lesions, shown by microscopy, which suggests the pathogenic mechanisms.

One adult female European mink (Mustela lutreola) was found dead during standard surveillance operations in which box traps were used; this trapping was part of biodiversity and ecology studies in the central part of the Danube delta in Romania (45°08′N, 29°19′E) in March 2010. The corpse was deep-frozen and analyzed after 3 months in the laboratory. During necropsy, multiple, well-defined, whitish nodules were observed in most muscular and subcutaneous tissues (Figure, panel A), with no evident preferential localization. We collected samples from these tissues for artificial digestion (9,10) and histologic examination, using the routine paraffin-embedding protocol and the following staining methods: hematoxylin-eosin, Masson trichrome, and Gordon and Sweet.

Artificial digestion released parasites (6 larvae/5 gm tissue) with typical larval trematode structures (Figure, panel B). By microscopy, we observed that morphologic features of these larvae were consistent with A. alata mesocercariae (6). Histopathologic examination confirmed the presence of parasitic forms in muscle sections (Figure, panel C). The mesocercariae were located in the connective fibrous tissue of the perimysium or between the muscle fibers. The typical structure of muscle fibers was altered around the larvae, with inflammatory cell reactions, represented mainly by lymphocytes, macrophages, and plasma cells (Figure, panel D). In other areas, the inflammatory reaction around the parasite was minimal or absent (Figure, panel E). In certain histologic sections, the damaged muscular tissue was replaced by granulation tissue in various stages of development (Figure, panel F). The maturity of the granulation tissue differed substantially, depending on the muscular areas examined. Some lesions were found in adult connective tissue, formed by mature collagen scar fibers (type I collagen) and few inflammatory cells, whereas other lesions had reticulin fibers (type III collagen) with numerous inflammatory cells. The lesions of the subcutaneous connective tissue consisted of an inflammatory reaction (panniculitis). The inflammation was characterized by a low number of mononuclear leukocytes and fibrinous exudate and fibroplasia.

The polyphasic nature of muscle and subcutaneous lesions produced by A. alata infection in its paratenic host appears to be caused by mesocercarial migration. This view is sustained by the presence of mononuclear cells that it infiltrates and by the appearance of the granulomatous tissue in various stages of maturation, which leads to muscle and subcutaneous fibroplasia. The reparatory nature of the lesions suggests that the inflammation is probably the result of direct tissue damage rather than an immune reaction targeted toward the parasitic antigens. This assumption could explain the local absence of inflammatory reaction around the parasites. The lack of inflammation was previously observed also with A. americana infection of humans (4). The structure of all mesocercariae observed by microscopy suggested that they were alive and active before the mink carcass was frozen. Because no mesocercariae were surrounded by adult connective tissue or by granulomatous inflammation, together with the multiple presences of migratory routes, the continuous mobility of the parasites through the host’s tissues was strongly suggested.

Although data on the pathologic changes caused by Alaria spp. in general, and A. alata parasites in particular, are scarce, the migration pattern and the lesions seem to be dependent on the particular parasite and host species. The reparatory nature of the lesions suggests that the inflammation is the result of direct tissue damage rather than an immune reaction targeted toward the parasitic antigens.



The research was conducted with the support of Unitatea Executivă pentru Finanțarea Învățământului Superior, a Cercetării, Dezvoltării și Inovării grant PCE236/2011.


Flaviu Tăbăran, Attila David SándorComments to Author , Mihai Marinov, Cornel Cătoi, and Andrei Daniel Mihalca
Author affiliations: University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, Cluj-Napoca, Romania (F. Tăbăran, A.D. Sándor, C. Cătoi, A.D. Mihalca); Danube Delta National Institute for Research and Development, Tulcea, Romania (M. Marinov)



  1. Möhl  K, Grosse  K, Hamedy  A, Wüste  T, Kabelitz  P, Lücker  E. Biology of Alaria spp. and human exposition risk to Alaria mesocercariae-a review. Parasitol Res. 2009;105:115. DOIPubMedGoogle Scholar
  2. Kramer  MH, Eberhard  ML, Blankenberg  TA. Respiratory symptoms and subcutaneous granuloma caused by mesocercariae: a case report. Am J Trop Med Hyg. 1996;55:4478 .PubMedGoogle Scholar
  3. McDonald  HR, Kazacos  KR, Schatz  H, Johnson  RN. Two cases of intraocular infection with Alaria mesocercaria (Trematoda). Am J Ophthalmol. 1994;117:44755 .PubMedGoogle Scholar
  4. Fernandes  BJ, Cooper  JD, Cullen  JB, Freeman  RS, Ritchie  AC, Scott  AA, Systemic infection with Alaria americana (Trematoda). Can Med Assoc J. 1976;115:11114 Scholar
  5. Freeman  RS, Stuart  PF, Cullen  SJ, Ritchie  AC, Mildon  A, Fernandes  BJ, Fatal human infection with mesocercariae of the trematode Alaria americana. Am J Trop Med Hyg. 1976;25:8037 .PubMedGoogle Scholar
  6. Skrjabin  KI, editor. Trematodes of animals and man; essentials of trematodology, vol. XVIII. Jerusalem (Israel): Program for Scientific Translations; 1965. p. 327–43.
  7. Anisimova  EI. Study on the European mink Mustela lutreola helminthocenoses in connection with the American mink M. vison expansion in the Belarus: story of the study and review of the results. Helminthologia. 2004;41:1936
  8. Odening  K. The “Duncker’s muscle fluke” can be transmitted experimentally to monkeys [in German]. Monatsh Veterinarmed. 1961;16:3959.
  9. Gamble  HR, Bessonov  AS, Cuperlovic  K, Gajadhar  AA, van Knapen  F, Noeckler  K. International Commission on Trichinellosis: recommendations on methods for the control of Trichinella in domestic and wild animals intended for human consumption. Vet Parasitol. 2000;93:39340. DOIPubMedGoogle Scholar
  10. Portier  J, Jouet  D, Ferté  H, Gibout  O, Heckmann  A, Boireau  P, New data in France on the trematode Alaria alata (Goeze, 1792) obtained during Trichinella inspections. Parasite. 2011;18:2715. DOIPubMedGoogle Scholar




Cite This Article

DOI: 10.3201/eid1909.130081

Related Links


Table of Contents – Volume 19, Number 9—September 2013

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.



Please use the form below to submit correspondence to the authors or contact them at the following address:

Attila D. Sándor, Department of Parasitology and Parasitic Diseases, University of Agricultural Sciences and Veterinary Medicine, Cluj-Napoca, Calea Mănăştur 3-5, RO-400372, Cluj, Romania

Send To

10000 character(s) remaining.


Page created: August 20, 2013
Page updated: August 20, 2013
Page reviewed: August 20, 2013
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.