Background: Infectious aetiology has been increasingly implicated as a potential contributor to intervertebral disc degeneration and the development of low back pain. While clinical observations suggest a role for bacterial pathogens in disc pathology, the precise mechanisms by which infection initiates and accelerates degeneration remain poorly defined. Experimental models are therefore essential to elucidate the causal relationship between infection and disc degeneration. 

Methods: A rabbit model was used to investigate the effects of bacterial inoculation on intervertebral disc degeneration. Eight male New Zealand rabbits were included. Two served as controls and received sham injections with tryptic soy broth (TSB), while the remaining six were divided into three groups (two rabbits per group). Clinical isolates of Pseudomonas aeruginosa, obtained from human disc specimens during surgery, were prepared at concentrations ranging from 1×10^7to 1×10^9CFU/ml. These inocula were injected into the nucleus pulposus of the L3–L4 discs. MRI imaging was performed at 1, 2, 4, and 8 weeks to monitor degenerative changes. At 8 weeks, animals were euthanised, and discs were harvested for histological analysis and bacterial culture. Microbial identification was confirmed using the VITEK 2 system. 

Results: Injection of P. aeruginosa consistently induced disc degeneration, with severity dependent on inoculum concentration. High-dose inoculation (1×10^9 CFU/mL) resulted in rapid degeneration of IVD within 1 week, which was evident on MRI. Lower doses (1×10^7–1×10^8 CFU/mL) produced similar degenerative changes more gradually, between two and four weeks. Subclinical infections, without overt systemic manifestations, nevertheless led to persistent disc degeneration. Histological analysis revealed marked neutrophil infiltration, destruction of the nucleus pulposus, and structural collapse of the disc, findings that correlated closely with MRI observations. 

Conclusion: This experimental rabbit model demonstrates that bacterial inoculation of the intervertebral disc reproducibly initiates and accelerates degeneration in a dose-dependent manner. High bacterial loads produced rapid and destructive changes, whereas lower inocula led to insidious, subclinical progression. These findings strengthen the hypothesis that infection may serve as a primary trigger of disc disease, while also providing a reproducible framework to study its pathophysiology