Retraction for Dinant et al., Aortic Homograft Endocarditis Caused by Campylobacter jejuni

RETRACTION

Volume 49, no. 11, p. 4016–4017, 2011. In our paper, we described the first case of homograft endocarditis caused by Campylobacter jejuni in a 46-year-old male. Only two other cases of C. jejuni endocarditis, involving native valves, had been reported before in the medical literature (A. Pönkä, T. Pitkänen, T. Pettersson, S. Aittoniemi, and T. U. Kosunen, Acta Med. Scand. 208:495–496, 1980; J. Torné Cachot, J. M. Garcés Jarque, R. Miralles Basseda, and A. García Flores, Rev. Clin. Esp. 184:114–115, 1989). The lightly curved, Gram-negative rods that grew from our patient's blood culture were oxidase, catalase, hippurate, and indoxylacetate positive, corresponding with Campylobacter jejuni.

In our laboratory, a PCR-based screening method for diarrheal pathogens (T. Schuurman, R. F. de Boer, E. van Zanten, K. R. van Slochteren, H. R. Scheper, B. G. Dijk-Alberts, A. V. Möller, and A. M. Kooistra-Smid, J. Clin. Microbiol. 45:3692–3700, 2007) was recently evaluated for use in routine diagnostics, and the collection of strains used in this evaluation included the strain from the C. jejuni endocarditis patient. To our surprise, the result for the PCR assay for C. jejuni on this strain was negative. The strain was further analyzed by DNA sequencing of 16S ribosomal RNA, which showed 100% homology with Campylobacter fetus. Additional PCR assays specifically designed for the identification of C. fetus (C. Tramuta, D. Lacerenza, S. Zoppi, M. Goria, A. Dondo, E. Ferroglio, P. Nebbia, and S. Rosati, J. Vet. Diagn. Invest. 23:657–664, 2011; C. Abril, E. M. Vilei, I. Brodard, A. Burnens, J. Frey, and R. Miserez, Clin. Microbiol. Infect. 13:993–1000, 2007; S. Hum, K. Quinn, J. Brunner, and S. L. On, Aust. Vet. J. 75:827–831, 1997) gave positive results. An amplified fragment length polymorphism (B. Duim, P. A. Vandamme, A. Rigter, S. Laevens, J. R. Dijkstra, and J. A. Wagenaar, Microbiology 147:2729–2737, 2001) also indicated C. fetus. Therefore, we have to conclude that the patient from our case report did not suffer from an endocarditis caused by C. jejuni but instead from an endocarditis caused by C. fetus, which is a much more common phenomenon, as was also discussed in the case report.

We subsequently repeated the phenotypic tests on the patient's strain. The result for the hippurate test was again positive, but the indoxylacetate test now gave a negative result. A positive hippurate test result would, however, already be sufficient to identify a campylobacter as C. jejuni (R. C. Jerris, P. I. Fields, and M. A. Nicholson, p. 3.8.2.10, in L. S. Garcia and H. D. Isenberg, ed., Clinical Microbiology Procedures Handbook, vol. 1, 2010). In a Dutch report, a multiplex PCR assay for diarrheal pathogens was compared to phenotypic identifications (M. T. van der Beek, W. van Pelt, L. Heres, K. Veldman, J. A. Wagenaar, W. F. Jacobs-Reitsma, D. J. Mevius, and E. J. Kuiper, Dutch J. Med. Microbiol., 17:6–12, 2009). The authors of that report analyzed 1,585 isolates from 8 different laboratories that were phenotypically identified as C. jejuni and found that 96% of these identifications were correct (range, 81 to 100%). A hippurate test result may be false positive when the final color after addition of the 3.5%-ninhydrin solution is examined after the maximum incubation time. In our laboratory, the time between the addition of the reagent and the examination of the final color is strictly set at 10 minutes. However, with the data from the report by van der Beek et al. in mind, we decided to send the isolate to two other laboratories in The Netherlands, one of which was the WHO Collaborating Center for Campylobacter. In both laboratories, the result for the hippurate test was negative. A negative result for a PCR assay for hipO (V. Caner, Y. Cokal, C. Cetin, A. Sen, and N. Karagenc, Antonie van Leeuwenhoek 94:527–532, 2008) confirmed this. Results for additional phenotypic tests, including tests for growth at 25°C (growth), growth at 42°C (no growth), and susceptibility to nalidixic acid (resistant) and cephalothin (sensitive), also matched C. fetus.

Our case underlines in general the importance of thorough confirmation of unexpected bacterial species in clinically important cases, either by molecular methods or by extensive and reliable phenotypic tests. More specifically, it underscores the previously reported unreliability of the phenotypic hippurate hydrolysis test for the correct identification of Campylobacter spp. We hereby retract the paper and sincerely apologize for the inconvenience caused to the readers.