Selective Pressure Promotes Tetracycline Resistance of Chlamydia Suis in Fattening Pigs

Abstract

In pigs, Chlamydia suis has been associated with respiratory disease, diarrhea and conjunctivitis, but there is a high rate of inapparent C. suis infection found in the gastrointestinal tract of pigs. Tetracycline resistance in C. suis has been described in the USA, Italy, Switzerland, Belgium, Cyprus and Israel. Tetracyclines are commonly used in pig production due to their broad-spectrum activity and relatively low cost. The aim of this study was to isolate clinical C. suis samples in cell culture and to evaluate their antibiotic susceptibility in vitro under consideration of antibiotic treatment on herd level.Swab samples (n = 158) identified as C. suis originating from 24 farms were further processed for isolation, which was successful in 71% of attempts with a significantly higher success rate from fecal swabs compared to conjunctival swabs. The farms were divided into three treatment groups: A) farms without antibiotic treatment, B) farms with prophylactic oral antibiotic treatment of the whole herd consisting of trimethoprime, sulfadimidin and sulfathiazole (TSS), or C) farms giving herd treatment with chlortetracycline with or without tylosin and sulfadimidin (CTS). 59 isolates and their corresponding clinical samples were selected and tested for the presence or absence of the tetracycline resistance class C gene [tet(C)] by conventional PCR and isolates were further investigated for their antibiotic susceptibility in vitro. The phenotype of the investigated isolates was either classified as tetracycline sensitive (Minimum inhibitory concentration [MIC] < 2 μg/ml), intermediate (2 μg/ml ≤ MIC < 4 μg/ml) or resistant (MIC ≥ 4 μg/ml). Results of groups and individual pigs were correlated with antibiotic treatment and time of sampling (beginning/end of the fattening period). We found clear evidence for selective pressure as absence of antibiotics led to isolation of only tetracycline sensitive or intermediate strains whereas tetracycline treatment resulted in a greater number of tetracycline resistant isolates.

The Chlamydia suis Genome Exhibits High Levels of Diversity, Plasticity, and Mobile Antibiotic Resistance: Comparative Genomics of a Recent Livestock Cohort Shows Influence of Treatment Regimes

“…Some discrepancies between the detection of tetA(C) by PCR and genomics were noted (table 1), corroborating previous findings (Donati et al. 2016; Wanninger et al. 2016).…”

“…Caution should be taken when using this as a diagnostic PCR for C. suis , especially as this gene is found in other bacteria and cloning vectors and its presence is not firmly related to in vitro susceptibility characteristics (Donati et al. 2016; Wanninger et al. 2016).…”

Isolation of Tetracycline-Resistant Chlamydia suis from a Pig Herd Affected by Reproductive Disorders and Conjunctivitis

“…A consensus MIC is necessary, because small discrepancies (2-fold differences) between assays are considered within the expected variations of these in vitro assays [19]. [35,36]) and were therefore confirmed to be resistant to tetracycline in vitro, while the MICs of tetA(C)-negative isolates (TcS), 330 MS and 490 MS, had MICs ranging from 0.06 to 0.125 µg/mL and were thus considered to be tetracycline sensitive. In contrast, no isolate showed in vitro resistance to doxycycline, although the MICs of TcR isolates were two-to eight-fold higher than those of TcS isolates (0.125-0.5 µg/mL compared to 0.06 µg/mL).…”

Development of aChlamydia suis-specific antibody enzyme-linked immunosorbent assay based on the use of a B-cell epitope of the polymorphic membrane protein C

“…Chlamydia suis infections could be successfully treated with tetracyclines until the appearance of a tetracycline resistant (Tc R ) phenotype, which was first isolated on pig farms in Iowa and Nebraska (Andersen & Rogers, ). Soon thereafter, tetracycline resistant C. suis strains appeared in other countries including Belgium, Cyprus, Germany, Israel, Italy, Switzerland and the Netherlands (Borel et al., ; Di Francesco et al., ; Donati et al., ; Schautteet et al., ; Vanrompay, 2016 unpublished results; Wanninger et al., ). Resistance was acquired via horizontal gene transfer of the class C gene [ tet (C)]‐containing cassette most likely from another gut bacterium in response to selective antibiotic pressure (Borel et al., ; Dugan, Rockey, Jones, & Andersen, ).…”