Sex Transm Infect 84:252-253 doi:10.1136/sti.2008.030148
  • Editorial

Lymphogranuloma venereum diagnostics: from culture to real-time quadriplex polymerase chain reaction

  1. Servaas A Morré1,2,3,
  2. Sander Ouburg1,3,
  3. Michiel A van Agtmael2,
  4. Henry J C de Vries4,5
  1. 1
    Laboratory of Immunogenetics, Section Immunogenetics of Infectious Diseases, Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands
  2. 2
    Section of Infectious Diseases, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands
  3. 3
    Department of Medical Microbiology, Maastricht University Medical Centre, Maastricht, The Netherlands
  4. 4
    Department of Dermatology, Academic Medical Centre, University of Amsterdam, The Netherlands
  5. 5
    STI Outpatient Clinic, Cluster of Infectious Diseases, Health Service Amsterdam, Amsterdam, The Netherlands
  1. Dr S A Morré, VU University Medical Center, Amsterdam, The Netherlands; samorretravel{at}
  • Accepted 18 June 2008

Since the end of 2003, an ongoing lymphogranuloma venereum (LGV) proctitis outbreak has been reported in industrialised countries, first in The Netherlands, followed by neighbouring European countries and the United Kingdom, and now in many other countries and continents including the United States, Canada and Australia.1 2

When we analysed the LGV strain identified in this outbreak on a nucleotide level, four nucleotide changes were found when compared with reference serovars (L2, L2a, and the variant L2′) including one change that encoded the previously undescribed change at amino acid 162, AAT→AGT and we designated this strain L2b (GenBank accession number AY586530).2 We have shown by retrospective epidemiological analyses that this L2b strain was the only strain present among men who have sex with men in Amsterdam and appeared to have been circulating in Amsterdam in 2000 (no retrospective samples were available before 2000).3 Moreover, we showed that this L2b variant was already present in the 1980s in San Francisco, with exactly the same mutations in the complete ompA gene (previously omp1).3

Since the identification of this at least 28-year slowly evolving …