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Background Data on antimicrobial resistance mechanisms are scanty for  Cedecea spp. , with very variable antibiotic resistance patterns documented. Here we report the first in vivo resistance evolution of a  C. davisae  clinical isolate in a patient with a complex hand trauma and provide insight in the resistance mechanism, leading to therapeutic implications for this pathogen. Case presentation Cedecea davisae  was isolated from a patient with hand trauma during a first surgical debridement. Six days after primary surgical treatment and under antimicrobial treatment with amoxicillin-clavulanic acid and later cefepime, follow up cultures yielded  C. davisae  which demonstrated a resistance development. The susceptible parental isolate and its resistant derivative were characterized by whole genome sequencing,  ampC, ompC and ompF  by RT- PCR. The resistant derivative demonstrated an A224G SNP in  ampD , the transcriptional regulator of  ampC , leading to a His75Arg change in the corresponding AmpD protein. AmpC transcription of the resistant derivative was 362-times higher than the susceptible isolate. Transcription levels of  ompF  and  ompC  were 8.5-fold and 1.3-fold lower, respectively, in the resistant derivative. Downregulation of OmpF putatively resulted from a mutation in the presumed promoter region upstream of the dusB-Fis operon, a proposed regulator for  ompF . Conclusions This case demonstrates the in vivo resistance development of  C. davisae  within 7 days similar to that of the members of the  Enterobacter cloacae  complex. Our findings add valuable information for future therapeutic management of these opportunistic pathogens as they warrant the same empirical treatment as AmpC producers.

AmpC hyperproduction in a Cedecea davisae implant-associated bone infection during treatment: a case report and therapeutic implications