Short Communication Evidence of feline herpesvirus-1 DNA in the vestibular ganglion of domestic cats Birgit Parzefall a , Wolfgang Schmahl a , Andrea Fischer b , Andreas Blutke a , Uwe Truyen c , Kaspar Matiasek d, * a Chairs of General Pathology and Neuropathology, Institute of Veterinary Pathology, Ludwig-Maximilians University, Munich, Germany b Section of Neurology, Department of Small Animal Medicine, Ludwig-Maximilians University, Munich, Germany c Institute of Animal Hygiene and Veterinary Public Health, University of Leipzig, Leipzig, Germany d Neuropathology Laboratory, Diagnostic Laboratory Services, The Animal Health Trust, Newmarket, UK article info Article history: Accepted 27 March 2009 Keywords: FHV-1 Feline herpesvirus Vestibular ganglion Labyrinth PCR abstract In humans, herpes simplex virus type-1 has recently been detected in the vestibular ganglion (VG) and labyrinth (VL) and may be associated with vestibular signs. Feline herpesvirus-1 (FHV-1) is widespread amongst cat populations and affects many different tissues. The aim of this pilot study was to investigate the presence of FHV-1 DNA in the VG and VL of randomly selected domestic cats using PCR. FHV-1 DNA was detected in the VG of 14% of the cats. There was no detectable FHV-1 DNA in the VL of any cat. None of the infected cats had vestibular signs related to the VG infection. Ó 2009 Elsevier Ltd. All rights reserved. Feline herpesvirus-1 (FHV-1) is a widespread alpha-herpesvirus causing acute upper respiratory tract and ocular disease in cats. More than 80% of cats become latent carriers after infection despite a specific immune response. The primary site of latency is consid- ered to be the trigeminal ganglion (TG). Reactivation and shedding of virus occur spontaneously or after stressful stimuli (Gaskell et al., 2007). Herpes simplex virus type-1 (HSV-1) has been de- tected in the vestibular ganglion (VG) and labyrinth (VL) in hu- mans. Reactivation of HSV-1 in the VG is assumed to cause vestibular neuritis, and benign paroxysmal positional vertigo could be a sequel of viral labyrinthitis (Arbusow et al., 2001). To date, none of these structures has been investigated for the presence of FHV-1 in healthy or diseased cats. This pilot study was launched to screen for FHV-1 DNA in the VG and VL of randomly selected domestic cats using PCR. Tissue specimens were obtained from 50 cats (31 males, 19 fe- males) presented to the Department of Small Animal Medicine, Ludwig-Maximilians University, Munich. All cats underwent post-mortem examination between 2007 and 2008. Their ages ran- ged from 4 weeks to 17 years (mean ± standard deviation [SD]: 6.82 ± 5.39 years). Altogether, the VL and the VG of 97 temporal bones and 60 TG were harvested as described elsewhere (Parzefall et al., 2009). All samples were collected within 48 h of death, snap frozen in liquid nitrogen, and stored at À80 °C. DNA extraction was performed with a commercial kit (DNA Micro Kit, Qiagen) followed by spectrophotometric measurement of total DNA content (Nano- Drop 1000, peQLab). The presence of amplifiable DNA was con- firmed by PCR of a 229 bp segment of the GAPDH gene (Gröne et al., 1996). For PCR-based detection of FHV-1, 0.3 lg of total DNA was used to amplify a 383 bp fragment of the FHV-1-thymi- dine-kinase-gene (Reubel et al., 1993). DNA extracted from FHV- 1 infected cultured cells was used as positive and water as negative target template in each PCR run. All clinical and pathological re- cords were screened for neurological and non-neurological dis- eases and the cat owners were questioned about the vaccination status. A mean DNA content of 2.8 lg (±0.9) was obtained from the VL, 4.5 lg (±1.1) from the VG, and 4.1 lg (±1.2) from the extracted por- tion of the TG. FHV-1 DNA was detected in the VG of 14% of the cats with a unilateral distribution in six and bilateral affection in one of the cats. Thirty-two percent of the examined cats harboured FHV-1 DNA in the TG. All bilaterally investigated TG were affected on both sides (Table 1). All available TG from VG-infected animals were po- sitive for FHV-1. Twenty-two percent of the TG positive temporal bones also exhibited FHV-1 in the VG. No FHV-1 DNA was detected in the VL of any cat. FHV-1 positive cats showed no sex predilection and ranged from 2.5 to 16 years of age (mean ± SD: 9.29 ± 4.64). All infected cats presented with systemic underlying diseases. The vaccination status is depicted in Table 2. The presence of viral DNA in the VG was not accompanied by related vestibular deficits. To date, the presence of FHV-1 in the VG of domestic cats has not been documented in the literature. In the present study, we identified FHV-1 in 14% of randomly collected cats; this incidence ranged slightly below infection rates that we and others have observed in the TG. Notably, in all cats for which the complete data set was obtainable, infection of VG was accompanied by involve- ment of the TG. On the contrary, 78% of temporal bones with 1090-0233/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2009.03.030 * Corresponding author. Tel.: +44 1638 750659; fax: +44 1638 555643. E-mail address: kaspar.matiasek@neuropath.org.uk (K. Matiasek). The Veterinary Journal 184 (2010) 371–372 Contents lists available at ScienceDirect The Veterinary Journal journal homepage: www.elsevier.com/locate/tvjl