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1 Department of Animal Sciences, Katholieke Universiteit Leuven, Kasteelpark Arenberg 21 (Laboratory of Gene Technology) and 30 (Laboratory of Physiology and Immunology of Domestic Animals), 3001 Leuven, Belgium
2 Department of Molecular Biotechnology, Ghent University, Coupure Links 653, 9000 Ghent, Belgium
3 Department of Clinical Microbiology, University Hospital, S-751 85 Uppsala, Sweden
4 Department of Microbiology, University of Georgia, Athens, GA 30602, USA
Correspondence
D. Vanrompay
Daisy.Vanrompay{at}rug.ac.be
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Published online ahead of print on 7 February 2003 as DOI 10.1099/ijs.0.02329-0.
The GenBank accession numbers for the sequences obtained in this study are AJ310735–AJ310737 and AF481048–AF481052, as detailed in Figs 2 and 3
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The sequence alignments used to generate the phylograms shown in Figs 2 and 3 are available as supplementary material in IJSEM Online.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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; Anderson et al., 1978; Edwards, 1981; Hedberg et al., 1989; Ni et al., 1996; Brewis & McFerran, 1997; Goupil et al., 1998; Bennedsen & Filskov, 2000; Centers for Disease Control and Prevention, 2000). Chlamydophila abortus causes abortion and foetal death in mammals, including humans (Wong et al., 1985; Jorgensen, 1997; Rodolakis et al., 1998). In the absence of sequence data, these species have no apparent relationship. Side-by-side comparisons of C. psittaci and C. abortus in birds and other animals show differences in infectivity, persistence, disease and seroconversion (Page, 1966; Johnson & Grimes, 1983; Tappe et al., 1989). Different mAbs recognize C. psittaci and C. abortus (Perez-Martinez & Storz, 1985; Eb et al., 1986; Fukushi et al., 1987; Takahashi et al., 1988; Andersen & Van Deusen, 1988; Kikuta et al., 1991; Andersen, 1991; Vretou et al., 1996). C. psittaci and C. abortus genomes exhibit different restriction endonuclease patterns (Herring et al., 1987; Timms et al., 1988; McClenaghan et al., 1991; Sayada et al., 1995). DNA–DNA reassociation studies show that C. psittaci and C. abortus are 27–85 % similar (Cox et al., 1988; Fukushi & Hirai, 1989). C. psittaci strains more often than not have an extrachromosomal plasmid, while C. abortus strains have no plasmid (Everett et al., 1999). The genetic criteria responsible for the differing pathogenicity of C. psittaci and C. abortus are not known, and the selective pressures that drive the separation of these species are not understood.
Isolates that do not conform to this picture have been described and in some cases, the inconsistencies have been resolved. For example, enzootic abortion of ewes (EAE) strain A22/M, which had characteristics of C. psittaci, was shown to be a culture contaminant when bona fide C. abortus A22 was sequenced (Bush & Everett, 2001). C. psittaci strain M56 was reported to have a serotype characteristic of Chlamydophila felis, using polyclonal sera (Fukushi & Hirai, 1988); M56 proved to be a mixed culture (Herrmann et al., 2000a). In other cases, inconsistencies have not been resolved. For example, strain R54, identified in a bird that was captured in the Antarctic, appeared to be related more closely to C. abortus than to C. psittaci (Herrmann et al., 2000b). C. psittaci strain Prk/Daruma was reported to have a C. felis serotype, using polyclonal sera (Fukushi & Hirai, 1988), but it was also recognized by avian mAbs (Fukushi et al., 1987). DNA–DNA reassociation data for Prk/Daruma were inconclusive (Fukushi & Hirai, 1989). Analysis of Prk/Daruma 16S rRNA shows that it is intermediate between those of C. psittaci and C. abortus (Pudjiatmoko et al., 1997). Prk/Daruma has a typical C. psittaci restriction enzyme ribosomal profile and a unique ompA AluI restriction enzyme profile (genotype F) (Fukushi et al., 1987; Fukushi & Hirai, 1988; Sayada et al., 1995; Everett & Andersen, 1999). The genotype F profile was also found in C. psittaci strains 10433-MA (Sayada et al., 1995) and 84/2334 (Vanrompay et al., 1997). Strain 84/2334 is recognized by serovar A mAbs, the same serotyping mAbs that recognize the C. psittaci type strain 6BCT and a large proportion of other C. psittaci isolates (Vanrompay et al., 1997).
Despite obvious pathological differences, analysis of gene sequences shows that C. psittaci comprises an unresolved cluster of strains, from which C. abortus is evolving (Bush & Everett, 2001). To clarify these relationships further, this study characterized genes from six C. psittaci isolates (84/2334, VS225, VS1, Prk/Daruma, MNRh and MNOs). These genes included ompA, rnpB and the rrn intergenic spacer. Furthermore, the presence of an extrachromosomal plasmid was investigated. Analysis and comparison of these genetic loci with those of other Chlamydophila strains, including C. abortus, reconciled inconsistencies in the existing data and allowed us to test the hypothesis that C. abortus is evolving from C. psittaci. These findings clarify the distinction of these two species and highlight the importance of identifying the genetic elements responsible for C. psittaci pathogenicity.
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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. Isolation and growth of C. psittaci strain 84/2334 was performed as described previously (Vanrompay et al., 1992, 1997). DNA templates were prepared as described previously (Everett et al., 1991; Herrmann et al., 2000a). DNA from strain 84/2334 was obtained using the Qiagen genomic DNA purification procedure. Extracts of a possible extrachromosomal plasmid were obtained from approximately 108 inclusion-forming units for each of strains 84/2334, 6BCT and B577T using the Qiagen TIP 500 plasmid midi kit.
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), X62475 (M. E. Lusher, J. Gregory, C. C. Storey & S. J. Richmond, unpublished) and X82078 (Thomas et al., 1997)] (Table 2). Eluates were PCR-amplified in 50 mM KCl, 20 mM Tris/HCl (pH 8·3), 2 mM MgCl2, 0·1 % Tween 20, 200 µM each dNTP, 20 µM each primer and 0·1 U SuperTaq polymerase (5 U µl-1). After an initial denaturation at 95 °C for 5 min, 30 cycles of 1 min at 95 °C, 2 min at 52 °C and 3 min at 72 °C were performed, with a final extension at 72 °C for 5 min. PCR products were detected after electrophoresis on a 1·2 % agarose gel by using ethidium bromide staining and UV illumination. A CE-LIF dsDNA 100 bp ladder (Bio-Rad) was used as a marker.
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). The C. psittaci strain 84/2334 ompA PCR product was cloned into pGEM-T (Promega), and clones with inserts were selected on Luria–Bertani/ampicillin/IPTG/X-Gal plates. White colonies were tested for insert size by PCR amplification using universal T7 and SP6 primers, and six clones that produced PCR products of approximately 1100 bp were selected for sequence characterization. Initial analysis of these clones indicated that they were apparently identical, so one was selected randomly for full-length sequencing.
Sequence analyses.
The sequence of the C. psittaci 84/2334 ompA clone was determined by using T7, SP6 and additional primers. The primers given in Table 2 were used for direct sequencing of the extrachromosomal plasmid, rrn spacer and rnpB PCR products after removal of amplification primers by filtration (Microcon 100 microconcentrators; Millipore). The dideoxynucleotide chain-termination method (Sanger et al., 1977) and Big Dye PCR cycle sequencing were used with ABI automated DNA sequencers (Applied Biosystems) to obtain sequence data from clones and from PCR products. All PCR products were sequenced on both strands.
Alignments and phylogenetic analyses.
The sequences of ompA, rnpB and the rrn spacer and the deduced amino acid sequence of the major outer-membrane protein (MOMP) were aligned with related sequences identified by using BLAST (http://www.ncbi.nlm.nih.gov). Multiple alignment was done with CLUSTAL X software (default settings) (Thompson et al., 1997) followed by manual editing; gapped positions were removed. Neighbour-joining (NJ) analysis was conducted with PAUP* 4.0b8 (Swofford, 2001) using heuristic searching to construct a 50 % majority-rule consensus tree for both the ompA gene and the intergenic spacer (100 replications, ACCTRAN character optimization, TBR+MULTREES branch-swapping option). Jukes–Cantor pairwise corrected distances were calculated for the ompA gene and the rrn spacer (Jukes & Cantor, 1969). Branching-order reliability was evaluated by 100 replications of bootstrap resampling. The sequence alignments are available as supplementary material in IJSEM Online.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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a). An extrachromosomal plasmid is often present in C. psittaci strains, but has not been found in C. abortus. This PCR did not generate a product from the C. abortus B577T template (Fig. 1a). Sequence analysis of the strain 84/2334 PCR product revealed that it was 469 bp long (Fig. 1b) and identical to a GenBank sequence for the C. psittaci extrachromosomal plasmid pCpA1 (strain N352, accession no. X62475). The 84/2334 sequence differed in four positions from the C. psittaci pAP'p plasmid sequence (accession no. M32753). The plasmid segments from 84/2334 and pCpA1 differed by approximately 25 % from the Chlamydophila caviae plasmid sequence (http://www.tigr.org/), 31 % from the Chlamydophila pecorum Koala II plasmid, 32 % from the C. pneumoniae N16 plasmid and 47 % from plasmids in Chlamydia trachomatis LGV440 and Chlamydia muridarum MoPn. This indicated that the C. psittaci-like extrachromosomal plasmid was present in strain 84/2334.
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), although some of the branches were delineated from relatively few additional nucleotide differences. Strains GP1 NGP-17/11-14, GP3 NPG-LX 603C-12, M1 Bab-mouse-5 and R1 PNT-7 Montana rabbit have rrn intergenic spacer sequences identical to those of C. abortus strains EBA, OSP, A22 and B577T. So, despite the diverse host spectrum, the rrn intergenic spacers of all sequenced C. abortus strains are identical. Divergence of the 84/2334 cluster from the Par1, 6BCT and MN clusters was evident from direct examination of the spacer sequence data, NJ analysis (Fig. 2) and the 850 bases available for the 23S rRNA immediately downstream (data available in GenBank; analysis not shown). Relative to other C. psittaci strains, SNPs in strain 84/2334 at positions 186, 200 and 206 and a gap at position 194 were in a conserved portion of the spacer that is predicted to form a stem with a complementary downstream segment for 23S rRNA processing (Everett & Andersen, 1997). SNPs at positions 49, 50 and 90 were in hypervariable regions.
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). Examination of the five ompA conserved segments (CS1–CS5) of C. psittaci and C. abortus strains showed few deduced amino acid differences but large numbers of nucleotide differences (Table 3). These nucleotide differences revealed the probable order of ompA divergence in Chlamydophila. NJ analysis of ompA CS sequences showed two C. psittaci lineages diverging: one contained the C. psittaci type strain 6BCT and MN strains, while the other contained numerous C. psittaci strains (including 84/2334) and C. abortus (Fig. 3a). In the latter lineage, WC, NJ1 and TT3 diverged early; C. psittaci strains Par1, GD and CT1 clustered together, and the Par1 cluster, VS225, 84/2334, R54 and C. abortus strains each diverged later and separately (Fig. 3a). Strains GP1 NGP-17/11-14, GP3 NPG-LX 603C-12, M1 Bab-mouse-5 and R1 PNT-7 Montana rabbit have ompA sequences identical to that of C. abortus strain EBA. So, despite a wide range of hosts, C. abortus strains have almost identical ompA sequences. Bootstrap resampling provided support for this branching order. Sequences of C. psittaci strains (CT1, Par1, GD, VS225, R54 and 6BCT) and of C. abortus strains (B577T and LLG) showed nucleotide differences with reference to C. psittaci strain 84/2334 that were distributed unevenly among the CS sequences; just 1/10 of the SNPs encoded amino acid changes. None of these differences encoded functionally divergent amino acids. Summing of the data in Table 3 provided a measure of this diversity: CS1 and CS5 had a total of 24 nucleotide differences that led to just five amino acid differences; CS2 and CS4 had 86 and 87 nucleotide differences, respectively, translating into a total of 11 amino acid differences. The 128 nucleotide differences in CS3 translated into 22 amino acid differences. The numbers of nucleotide and amino acid differences showed no correlation with insertion/deletion (indel) size or with apparent phylogeny (Table 3). All available C. abortus ompA sequences differed from the CS sequences of even the most closely related C. psittaci strains (including strain R54) by 16 unique point mutations.
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). NJ analysis of the VS sequences was generally consistent with analysis of the CS sequences, except in the case of strain VS225 (Fig. 3a, b). Like CS analysis, NJ analysis of the VS sequences showed two major lineages. One lineage contained C. psittaci 6BCT and MN strains, whereas the other contained C. psittaci strains CT1, Par1, GD, R54, VS225 and 84/2334, from which C. abortus diverged last. The VS sequences of strains WC, TT3 and NJ1 branched separately. Divergence of strain VS225, according to VS analysis, occurred just before the separation of C. abortus; according to CS analysis, however, strain VS225 separated several nodes closer to the base of the C. psittaci lineage. Strain 84/2334 shared eight VS point mutations with all members of the Par1/GD/CT1 cluster to the exclusion of all other strains; strain WC had four of the divergent Par-cluster bases (in VS2). Strain R54 had six point mutations (in VS1) that grouped it with the Par cluster; four mutations (VS3 and VS4) grouped R54 with C. abortus and were also present in 84/2334. C. abortus shared a set of 15 exclusive VS point mutations with 84/2334 and 11 of these with VS225. C. abortus VS sequences were uniquely distinguished from all C. psittaci strains by four point mutations. The downstream non-coding segment between ompA and tRNAGly also revealed an order of divergence that was congruent with the CS divergence (data available in GenBank; analysis not shown).
Hypervariable segment diversity in rnpB
The PCR-amplified 388 bp portion of rnpB from C. psittaci strain 84/2334 was identical in sequence to that of strain R54 and differed by an SNP and a 2-base deletion from the sequence of C. abortus strain B577T (Fig. 4). The 2-base deletion in 84/2334 was conserved among nine available C. psittaci rnpB sequences described by Herrmann et al. (2000a) (strains 6BCT, GD, NJ1, WC, VS225, 360, N352, Cal10 and CP3). Strain 84/2334 rnpB differed from all nine C. psittaci sequences by 6 bases in four previously described rnpB hypervariable regions (P3, P12, P17 and P19; Fig. 4) (Herrmann et al., 2000a).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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). In view of this, it is particularly intriguing that strain R54 was obtained in Antarctica from a brown skua. This bird breeds in the Southern Ocean from New Zealand to the Falklands and migrates to the Northern Hemisphere during the southern winter (Hermann et al., 2000b). Thus, it is no surprise that isolates as closely related as Par1, GD and CT1 could be found in such diverse respective hosts and locations as a partridge in Britain, a duck in Germany and a turkey in California. Remarkably, only C. psittaci has been identified in birds, to date (Everett et al., 1999). C. psittaci strains in birds infect mucosal epithelial cells and macrophages of the respiratory tract. Septicaemia eventually develops and the bacteria become localized in epithelial cells and macrophages of various organs (Vanrompay et al., 1995).
All C. abortus strains that have been characterized or identified were isolated or PCR-amplified from placenta or foetal organs after spontaneous abortion (Rodolakis et al., 1998). C. abortus is transmitted orally and sexually among mammals. C. abortus infection generally remains unapparent until an animal aborts late in gestation or gives birth to a weak or dead foetus. Infected females are most likely to shed bacteria near the time of ovulation. C. abortus strains are endemic among ruminants and have been associated with abortion in a horse, a rabbit, guinea pigs, mice, pigs and humans (Table 1) (Rodolakis et al., 1998; Everett et al., 1999; Pospischil et al., 2002). C. abortus has not been isolated from birds. C. psittaci and C. abortus were recognized as species primarily on the basis of differences in pathogenicity and DNA–DNA reassociation (Cox et al., 1988; Fukushi & Hirai, 1989; Everett et al., 1999).
In this report, we have presented evidence for the divergence of C. abortus from C. psittaci. Conservation in rnpB, ompA and rrn gene sequences of C. psittaci and C. abortus indicated that these species once shared a common ancestor. Divergence from this ancestor was evident in conserved segments of the ompA gene, in the rrn intergenic spacer and in additional segments. C. psittaci strains WC, NJ1 and TT3 had diverged the least from this common ancestor, while two C. psittaci lineages had undergone extensive divergence. One lineage contained 6BCT and MN strains. The other lineage comprised progressively diverse strains, in which 84/2334, Prk/Daruma and R54 were intermediates in the evolution of C. abortus from C. psittaci and demonstrated characteristics of both species. The virtual absence of shared unique SNPs in conserved genetic loci of C. psittaci and C. abortus indicated that these strains did not diverge recently.
C. psittaci strain 84/2334 provides a link that was previously missing in our understanding of the divergence of C. abortus from the C. psittaci lineage. C. psittaci strain 84/2334 had DNA sequence identity with an extrachromosomal plasmid in duck strain N352 (pCpA1; Thomas et al., 1997), with rnpB in strain R54 from a brown skua (originally characterized as C. abortus; Herrmann et al., 2000b) and with the rrn intergenic spacer in parakeet strain Prk/Daruma (Fig. 2) (Fukushi et al., 1987). These data confirmed the relatedness among these C. psittaci strains, while the accumulation of SNPs in ompA CS sequences suggested the antiquity of their separation (Table 3). Although C. psittaci ompA was heterogeneous and highly diverged, all available C. abortus ompA sequences differed from the CS sequences of even the most closely related C. psittaci strains (including R54) by 16 SNPs. Total ompA CS nucleotide differences between C. psittaci strain 84/2334, C. psittaci and C. abortus, shown in Table 3 and in the NJ analysis (Fig. 3a), support the intermediate position of strains 84/2334, Prk/Daruma and R54 in the evolution of C. abortus from C. psittaci. The NJ tree of ompA CS sequences shows a strong resemblance to the quartet puzzling phylogenetic tree based on MOMP sequences described by Bush & Everett (2001).
Comparison of nucleotide sequences for the CS and VS sequences of ompA revealed the effects of selective pressures. C. psittaci strains VS225 and 84/2334 shared 11 unique VS point mutations with C. abortus, despite all other loci showing VS225 diverging early and 84/2334 as an intermediate (Fig. 3). Strain R54 shared only two of the 11 C. abortus VS mutations. This suggests that C. psittaci strain VS225 has evolved toward the C. abortus-like genotype, whereas strains R54 and 84/2334 have not. Such evidence is masked when comparisons look only at indels, amino acids, parsimony or NJ analysis of the entire ompA. Because the history of the evolution of these strains is not available to us, we cannot know what selective forces caused VS evolution in strain VS225 towards C. abortus. It has been proposed that random accumulation of nucleotide changes provides a fertile structural substrate of hypervariability (Chang & Casali, 1994). Accumulation of mutations in C. psittaci ompA has certainly provided a coding sequence prone to replacement mutations and amino acid substitutions. The discovery of convergent evolution in VS225 triggers important considerations, since VS regions are often relied upon for identifying chlamydiae through sequence analysis, RFLP (Vanrompay et al., 1997) and mAb recognition. Reliance on such highly divergent sequences for classification can result in mistaken identification, as in the recent assignment of strain R54 to C. abortus (Herrmann et al., 2000b). On the basis of our new understanding of these lineages, we hereby move R54 from C. abortus to C. psittaci.
Our findings of diversity and evolution in C. psittaci are consistent with reports based on 16S rRNA analysis (Pudjiatmoko et al., 1997; Takahashi et al., 1997; Pettersson et al., 1997; Everett et al., 1999; Bush & Everett, 2001). (Pudjiatmoko et al. 1997) suggested that C. psittaci strain Prk/Daruma (D85710) was intermediate between C. psittaci and C. abortus, and Takahashi et al. (1997) had evidence for three intermediate isolates from parakeets (Prk 46, accession no. AB001809; Prk 48, accession no. AB001810; Prk 49, accession no. AB001811). CLUSTAL X analysis of these four strains shows that their 16S rRNA sequences are identical (data not shown) (Pudjiatmoko et al., 1997; Takahashi et al., 1997).
How does a bacterium that causes systemic disease in birds evolve into an agent of mammalian abortion? The answer will provide critical insights into the mechanisms of chlamydial virulence, and may eventually only be answered by genome sequence comparison. Until typing methods are expanded, our ability to distinguish C. psittaci and C. abortus will continue to rely on ecological differences, mAbs and genetic data (16S or 23S rRNA signature sequences, ompA, cysteine-rich proteins, kdtA or groEL) (Everett & Andersen, 1997; Meijer et al., 1997, 1999; Takahashi et al., 1997; Wardrop et al., 1999; Herrmann et al., 2000a; Ochiai et al., 2000; Bush & Everett, 2001). Because of this, we must utilize more than a single method and more than a single gene to characterize novel strains. Our study suggests that there is much to be learned about the separation of C. psittaci and C. abortus.
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ACKNOWLEDGEMENTS |
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
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Andersen, A. A. & Van Deusen, R. A. (1988). Production and partial characterization of monoclonal antibodies to four Chlamydia psittaci isolates. Infect Immun 56, 2075–2079.
Andersen, A. A., Grimes, J. E. & Shivaprasad, H. L. (1998). Serotyping of Chlamydia psittaci isolates from ratites. J Vet Diagn Invest 10, 186–188.
Anderson, D. C., Stoesz, P. A. & Kaufmann, A. F. (1978). Psittacosis outbreak in employees of a turkey-processing plant. Am J Epidemiol 107, 140–148.
Baehr, W., Zhang, Y.-X., Joseph, T., Su, H., Nano, F. E., Everett, K. D. E. & Caldwell, H. D. (1988). Mapping antigenic domains expressed by Chlamydia trachomatis major outer membrane protein genes. Proc Natl Acad Sci U S A 85, 4000–4004.
Bennedsen, M. & Filskov, A. (2000). An outbreak of psittacosis among employees at a poultry abattoir. In Proceedings of the 4th Meeting of the European Society for Chlamydia Research, Helsinki, Finland, August 20–23 2000, p. 315.
Brewis, C. & McFerran, D. J. (1997). ‘Farmer's ear': sudden sensorineural hearing loss due to Chlamydia psittaci infection. J Laryngol Otol 111, 855–857.[Medline]
Brown, J. W. (1998). The ribonuclease P database. Nucleic Acids Res 26, 351–352.
Bush, R. M. & Everett, K. D. E. (2001). Molecular evolution of the Chlamydiaceae. Int J Syst Evol Microbiol 51, 203–220.[Abstract]
Centers for Disease Control and Prevention (2000). Compendium of measures to control Chlamydia psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis). MMWR Recomm Rep 49 (RR-8), 3–17.[Medline]
Chang, B. & Casali, P. (1994). The CDR1 sequences of a major proportion of human germline Ig VH genes are inherently susceptible to amino acid replacement. Immunol Today 15, 367–373.[CrossRef][Medline]
Cox, R. L., Kuo, C.-C., Grayston, J. T. & Campbell, L. A. (1988). Deoxyribonucleic acid relatedness of Chlamydia sp. strain TWAR to Chlamydia trachomatis and Chlamydia psittaci. Int J Syst Bacteriol 38, 265–268.
Durfee, P. T., Pullen, M. M., Currier, R. W., II & Parker, R. L. (1975). Human psittacosis associated with commercial processing of turkeys. J Am Vet Med Assoc 167, 804–808.[Medline]
Eb, F., Orfila, J., Milon, A. & Geral, M. F. (1986). Epidemiologic significance of the immunofluorescence typing of Chlamydia psittaci. Ann Inst Pasteur Microbiol 137B, 77–93 (in French).[CrossRef]
Edwards, W. A. (1981). Ornithosis in poultry workers. Vet Rec 108, 155.[Medline]
Everett, K. D. E. & Andersen, A. A. (1997). The ribosomal intergenic spacer and domain I of the 23S rRNA gene are phylogenetic markers for Chlamydia spp. Int J Syst Bacteriol 47, 461–473.
Everett, K. D. E. & Andersen, A. A. (1999). Identification of nine species of the Chlamydiaceae using PCR-RFLP. Int J Syst Bacteriol 49, 803–813.
Everett, K. D. E., Andersen, A. A., Plaunt, M. & Hatch, T. P. (1991). Cloning and sequence analysis of the major outer membrane protein gene of Chlamydia psittaci 6BC. Infect Immun 59, 2853–2855.
Everett, K. D. E., Bush, R. M. & Andersen, A. A. (1999). Emended description of the order Chlamydiales, proposal of Parachlamydiaceae fam. nov. and Simkaniaceae fam. nov., each containing one monotypic genus, revised taxonomy of the family Chlamydiaceae, including a new genus and five new species, and standards for the identification of organisms. Int J Syst Bacteriol 49, 415–440.
Fukushi, H. & Hirai, K. (1988). Immunochemical diversity of the major outer membrane protein of avian and mammalian Chlamydia psittaci. J Clin Microbiol 26, 675–680.
Fukushi, H. & Hirai, K. (1989). Genetic diversity of avian and mammalian Chlamydia psittaci strains and relation to host origin. J Bacteriol 171, 2850–2855.
Fukushi, H., Nojiri, K. & Hirai, K. (1987). Monoclonal antibody typing of Chlamydia psittaci strains derived from avian and mammalian species. J Clin Microbiol 25, 1978–1981.
Goupil, F., Pelle-Duporte, D., Kouyoumdjian, S., Carbonelle, B. & Tuchais, E. (1998). Severe pneumonia with a pneumococcal aspect during an ornithosis outbreak. Presse Med 27, 1084–1088 (in French).
Hedberg, K., White, K. E., Forfang, J. C., Korlath, J. A., Friendshuh, K. A. J., Hedberg, C. W., MacDonald, K. L. & Osterholm, M. T. (1989). An outbreak of psittacosis in Minnesota turkey industry workers: implications for modes of transmission and control. Am J Epidemiol 130, 569–577.
Herring, A. J., Anderson, I. E., McClenaghan, M., Inglis, N. F., Williams, H., Matheson, B. A., West, C. P., Rodger, M. & Brettle, P. P. (1987). Restriction endonuclease analysis of DNA from two isolates of Chlamydia psittaci obtained from human abortions. Br Med J (Clin Res Ed) 295, 1239.
Herrmann, B., Pettersson, B., Everett, K. D. E., Mikkelsen, N. E. & Kirsebom, L. A. (2000a). Characterization of the rnpB gene and RNase P RNA in the order Chlamydiales. Int J Syst Evol Microbiol 50, 149–158.[Abstract]
Herrmann, B., Rahman, R., Bergström, S., Bonnedahl, J. & Olsen, B. (2000b). Chlamydophila abortus in a Brown skua (Catharacta antarctica lonnbergi) from a subantarctic island. Appl Environ Microbiol 66, 3654–3656.
Hugall, A., Timms, P., Girjes, A. A. & Lavin, M. F. (1989). Conserved DNA sequences in chlamydial plasmids. Plasmid 22, 91–98.[CrossRef][Medline]
Johnson, M. C. & Grimes, J. E. (1983). Resistance of wild birds to infection by Chlamydia psittaci of mammalian origin. J Infect Dis 147, 162.[Medline]
Jorgensen, D. M. (1997). Gestational psittacosis in a Montana sheep rancher. Emerg Infect Dis 3, 191–194.[Medline]
Jukes, T. H. & Cantor, C. R. (1969). Evolution of protein molecules. In Mammalian Protein Metabolism, vol. III, pp. 21–132. Edited by H. N. Munro. New York: Academic Press.
Kikuta, A., Furukawa, N., Yoshida, T., Fukushi, H., Yamaguchi, T. & Hirai, K. (1991). Antigenic analysis of avian Chlamydia psittaci using monoclonal antibodies to the major outer membrane protein. J Vet Med Sci 53, 385–389.[Medline]
McClenaghan, M., Inglis, N. F. & Herring, A. J. (1991). Comparison of isolates of Chlamydia psittaci of ovine, avian and feline origin by analysis of polypeptide profiles from purified elementary bodies. Vet Microbiol 26, 269–278.[CrossRef][Medline]
Meijer, A., Kwakkel, G. J., de Vries, A., Schouls, L. M. & Ossewaarde, J. M. (1997). Species identification of Chlamydia isolates by analyzing restriction fragment length polymorphism of the 16S-23S rRNA spacer region. J Clin Microbiol 35, 1179–1183.
Meijer, A., Morré, S. A., Van Den Brule, A. J. C., Savelkoul, P. H. M. & Ossewaarde, J. M. (1999). Genomic relatedness of Chlamydia isolates determined by amplified fragment length polymorphism analysis. J Bacteriol 181, 4469–4475.
Ni, A. P., Lin, G. Y., Yang, L. & 9 other authors (1996). A seroepidemiologic study of Chlamydia pneumoniae, Chlamydia trachomatis and Chlamydia psittaci in different populations on the mainland of China. Scand J Infect Dis 28, 553–557.[Medline]
Ochiai, Y., Fukushi, H., Yan, C., Yamaguchi, T. & Hirai, K. (2000). Comparative analysis of the putative amino acid sequences of chlamydial heat shock protein 60 and Escherichia coli GroEL. J Vet Med Sci 62, 941–945.[CrossRef][Medline]
Page, L. A. (1966). Interspecies transfer of psittacosis-LGV-trachoma agents: pathogenicity of two avian and two mammalian strains for eight species of birds and mammals. Am J Vet Res 27, 397–407.[Medline]
Perez-Martinez, J. A. & Storz, J. (1985). Antigenic diversity of Chlamydia psittaci of mammalian origin determined by microimmunofluorescence. Infect Immun 50, 905–910.
Pettersson, B., Andersson, A., Leitner, T., Olsvik, Ø., Uhlén, M., Storey, C. & Black, C. M. (1997). Evolutionary relationships among members of the genus Chlamydia based on 16S ribosomal DNA analysis. J Bacteriol 179, 4195–4205.
Pospischil, A., Thomas, R., Hilbe, M., Grest, P. & Gebbers, J.-O. (2002). Abortion in woman caused by caprine Chlamydophila abortus (Chlamydia psittaci serovar 1). Swiss Med Wkly 132, 64–66.[Medline]
Pudjiatmoko Fukushi, H., Ochiai, Y., Yamaguchi, T. & Hirai, K. (1997). Phylogenetic analysis of the genus Chlamydia based on 16S rRNA gene sequences. Int J Syst Bacteriol 47, 425–431.
Rodolakis, A., Salinas, J. & Papp, J. (1998). Recent advances on ovine chlamydial abortion. Vet Res 29, 275–288.[Medline]
Sanger, F., Nicklen, S. & Coulson, A. R. (1977). DNA sequencing with chain-terminating inhibitors. Proc Natl Acad Sci U S A 74, 5463–5467.
Sayada, C., Andersen, A. A., Storey, C. C., Milon, A., Eb, F., Hashimoto, N., Hirai, K., Elion, J. & Denamur, E. (1995). Usefulness of omp1 restriction mapping for avian Chlamydia psittaci isolate differentiation. Res Microbiol 146, 155–165.[Medline]
Swofford, D. L. (2001). PAUP*. Phylogenetic analysis using parsimony (*and other methods). Sunderland, MA: Sinauer.
Takahashi, T., Takashima, I. & Hashimoto, N. (1988). Immunotyping of Chlamydia psittaci by indirect immunofluorescence antibody test with monoclonal antibodies. Microbiol Immunol 32, 251–263.[Medline]
Takahashi, T., Masuda, M., Tsuruno, T., Mori, Y., Takashima, I., Hiramune, T. & Kikuchi, N. (1997). Phylogenetic analyses of Chlamydia psittaci from birds based on 16S rRNA gene sequence. J Clin Microbiol 35, 2908–2914.
Tappe, J. P., Andersen, A. A. & Cheville, N. F. (1989). Respiratory and pericardial lesions in turkeys infected with avian or mammalian strains of Chlamydia psittaci. Vet Pathol 26, 386–395.[Abstract]
Thomas, N. S., Lusher, M., Storey, C. C. & Clarke, I. N. (1997). Plasmid diversity in Chlamydia. Microbiology 143, 1847–1854.
Thompson, J. D., Gibson, T. J., Plewniak, F., Jeanmougin, F. & Higgins, D. G. (1997). The CLUSTAL_X windows interface: flexible strategies for multiple sequence alignment aided by quality analysis tools. Nucleic Acids Res 25, 4876–4882.
Timms, P., Eaves, F. W., Girjes, A. A. & Lavin, M. F. (1988). Comparison of Chlamydia psittaci isolates by restriction endonuclease and DNA probe analyses. Infect Immun 56, 287–290.
Vanrompay, D., Ducatelle, R. & Haesebrouck, F. (1992). Diagnosis of avian chlamydiosis: specificity of the modified Giménez staining on smears and comparison of the sensitivity of isolation in eggs and three different cell cultures. Zentbl Veterinarmed B 39, 105–112.
Vanrompay, D., Mast, J., Ducatelle, R., Haesebrouck, F. & Goddeeris, B. (1995). Chlamydia psittaci in turkeys: pathogenesis of infections in avian serovars A, B and D. Vet Microbiol 47, 245–256.[CrossRef][Medline]
Vanrompay, D., Butaye, P., Sayada, C., Ducatelle, R. & Haesebrouck, F. (1997). Characterization of avian Chlamydia psittaci strains using omp1 restriction mapping and serovar-specific monoclonal antibodies. Res Microbiol 148, 327–333.[Medline]
Vretou, E., Loutrari, H., Mariani, L. & 7 other authors (1996). Diversity among abortion strains of Chlamydia psittaci demonstrated by inclusion morphology, polypeptide profiles and monoclonal antibodies. Vet Microbiol 51, 275–289.[CrossRef][Medline]
Wardrop, S., Fowler, A., O'Callaghan, P., Giffard, P. & Timms, P. (1999). Characterization of the koala biovar of Chlamydia pneumoniae at four gene loci – ompAVD4, ompB, 16S rRNA, groESL spacer region. Syst Appl Microbiol 22, 22–27.[Medline]
Wong, S. Y., Gray, E. S., Buxton, D., Finlayson, J. & Johnson, F. W. (1985). Acute placentitis and spontaneous abortion caused by Chlamydia psittaci of sheep origin: a histological and ultrastructural study. J Clin Pathol 38, 707–711.
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