However, the fact that a few isolates of K. oxytoca were isolated from other tissues, including palpebral conjunctiva, tumor, and, mammary gland, indicates that K. oxytoca can also colonize other organs. Antibiotic resistance patterns appear to vary considerably among different strains of K. oxytoca. Strains of K. oxytoca are resistant to amino-penicillins and carboxy-penicillins due to the production of b-lactamases. Antimicrobial susceptibility testing indicated that all of the K. oxytoca strains investigated were resistant to ampicillin, suggesting these isolates of K.oxytoca are able to synthesize B-lactamases. This is consistent with the presence of beta-lactamases that encode a gene present in the genome of K. oxytoca 09-7231. Resistance to amoxicillin/ clavuranate was also observed in select strains of K. oxytoca. Interestingly, K. oxytoca isolates originating from non-human primates Sulfanilamide showed resistance not only to ampicillin, cephalothin and amoxicillin/clavuranate, but also to trimethoprim/sulfamethoxazole, enrofloxacin, and gentamicin. The high percentage of antibiotic-resistant strains of K. oxytoca isolated from nonhuman primates may indicate the liberal use of antibiotics in primates, particularly when the animals are in Procainamide hydrochloride quarantine and placed on prophylactic antibiotics prior to release for research purposes. Genomic analysis of a cytotoxin-positive K. oxytoca isolated from a clinically affected mouse revealed homologs of multiple genes that promote pathogenicity in other pathogens. These include type I, type IV, and type VI secretion systems. The type IV secretion system promotes pathogenicity in H. pylori through injection of cagA. More recently, the type VI secretion system has been demonstrated to promote bacterial competition, host cell adhesion, and invasion in Escherichia coli, Campylobacter jejuni, Salmonella spp. In clinical isolates of K. pneumoniae, cultured from a liver abscess in a human, genes involved in allantoin metabolism were highly and uniquely upregulated, while the non-clinical strain of K. pneumoniae lacked genes involved in this metabolic pathway. The mouse clinical isolate of K. oxytoca investigated in this study also contains a large number of genes involved in allantoin metabolism, including alls and allr, which were found in the pathogenic strain of K. pneumoniae.