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Volume 18, Number 12—December 2012

Letter

Wild Boars as Hosts of Human-Pathogenic Anaplasma phagocytophilum Variants

Suggested citation for this article

To the Editor: Michalik et al. (1) reported a 12% prevalence of Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis and tick-borne fever of ruminants, in wild boars in Poland. A. phagocytophilum has been reported with low prevalence among wild boar in the Czech Republic, Slovenia (2), and Japan (3). In Spain and Mississippi, United States, A. phagocytophilum in wild boars or feral pigs, respectively, has not been reported (4,5). Furthermore, in Slovenia and Poland, the A. phagocytophilum gene sequences found in samples from wild boars were identical to those found in samples from humans and the tick vector Ixodes ricinus (1). These results suggested, as pointed out by Michalik et al. (1), that wild boar might play a role in the epizootiology of A. phagocytophilum by serving as a natural reservoir host, at least in some regions.

To test this hypothesis, we conducted transcriptomics studies to characterize host response to A. phagocytophilum infection in naturally and experimentally infected boars (6,7). The results suggested that boars are susceptible to A. phagocytophilum, but are able to control infection, mainly through activation of innate immune responses and cytoskeleton rearrangement to promote phagocytosis and autophagy. Control of A. phagocytophilum infection in boars might result in infection levels below PCR detection or infection clearance, contributing to the low percentage of infection prevalence detected for this species in most regions.

The low detection levels suggest that boars have a low or no impact as a reservoir host for A. phagocytophilum. Even if boars remain persistently infected with A. phagocytophilum at low levels by downregulating some adaptive immune genes and delaying the apoptotic death of neutrophils through activation of the Jak-STAT pathway, among other mechanisms (6), their role as a source of infection for ticks remains to be demonstrated.

José de la FuenteComments to Author  and Christian Gortazar
Author affiliations: Author affiliations: Instituto de Investigación en Recursos Cinegéticos, Ciudad Real, Spain (J. de la Fuente, C. Gortazar); Oklahoma State University, Stillwater, Oklahoma, USA (J. de la Fuente)

References

  1. Michalik J, Stańczak J, Cieniuch S, Racewicz M, Sikora B, Dabert M. Wild boars as hosts of human-pathogenic Anaplasma phagocytophilum variants.Emerg Infect Dis. 2012;18:9981001. DOIPubMed
  2. Strasek Smrdel K, Tozon N, Duh D, Petrovec M, Avsic Zupanc T. Diversity of groESL sequences of Anaplasma phagocytophilum among dogs in Slovenia.Clin Microbiol Infect. 2009;15(Suppl 2):7980. DOIPubMed
  3. Masuzawa T, Uchishima Y, Fukui T, Okamoto Y, Muto M, Koizumi N, Detection of Anaplasma phagocytophilum from wild boars and deer in Japan.Jpn J Infect Dis. 2011;64:3336.PubMed
  4. Portillo A, Pérez-Martínez L, Santibáñez S, Santibáñez P, Palomar AM, Oteo JA. Anaplasma spp. in wild mammals and Ixodes ricinus from the north of Spain.Vector Borne Zoonotic Dis. 2011;11:38. DOIPubMed
  5. Castellaw AH, Chenney EF, Varela-Stokes AS. Tick-borne disease agents in various wildlife from Mississippi.Vector Borne Zoonotic Dis. 2011;11:43942. DOIPubMed
  6. Galindo RC, de la Fuente J. Transcriptomics data integration reveals Jak-STAT as a common pathway affected by pathogenic intracellular bacteria in natural reservoir hosts.J Proteomics Bioinform.2012;5:10815.
  7. Galindo RC, Ayllón N, Strašek Smrdel K, Boadella M, Beltrán-Beck B, Mazariegos M, Gene expression profile suggests that pigs (Sus scrofa) are susceptible to Anaplasma phagocytophilum but control infection.Parasit Vectors.2012;5:181. DOIPubMed

Suggested citation for this article: de la Fuente J, Gortazar C. Wild boars as hosts of human-pathogenic Anaplasma phagocytophilum variants [letter]. Emerg Infect Dis [Internet]. 2012 Dec [date cited]. http://dx.doi.org/10.3201/eid1812.120778

DOI: 10.3201/eid1812.120778

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Table of Contents – Volume 18, Number 12—December 2012

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Jose de la Fuente, Department of Veterinary Pathobiology, College of Veterinary Medicine, 250 McElroy Hall, Oklahoma State University, Stillwater, OK 74078, USA

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