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Infection in the spine might be the cause of symptoms in a group of patients with severe chronic low back pain (LBP). What about the large body of research recommending biopsychosocial management? Where have we heard a similar story before? Well, Helicobacter pylori infection as the cause of indigestion was a major challenging discovery that led to a paradigm shift in managing that condition which had hitherto been managed mainly through symptomatic and psychological approaches, and sometimes major surgery. The similarities between these stories are uncanny—not least in the challenges facing attempts to establish the clear evidence. So what are the challenges that face proving the principle of infection theory in LBP? Following the Koch’s postulates linking infection and a disease state [1], we have to demonstrate that an infectious agent is present. Intact intervertebral discs are avascular and sterile but pathogens have been identified in herniated and degenerated discs since the 1970s [2, 3]. Compared to the stomach, access to intervertebral discs is difficult and sampling carries a high risk of contamination from the skin. This is particularly relevant as the most common pathogens isolated are Propionibacterium acnes and coagulase negative Staphylococci, both common skin commensals. Two recent reviews conclude that micro-organisms are found in about 35 % of surgically removed discs, and that P. acnes is the most frequently identified species [4, 5]. When samples are taken from the vertebral body rather than from the disc, no evidence of bacteria can be found [6]. In 1987, particular signs or changes seen on magnetic resonance imaging (MRI) of the spine were described for the first time [7], Michael Modic then classified them into three types with distinct radiological and histological features [8]. Type 1 Modic changes correspond to bone oedema of the vertebral endplate; type 2 fatty degeneration and type 3 end-stage sclerosis. These changes are thought to be caused by inflammatory mediators in the adjacent herniated or degenerated discs triggered by infection in these discs. In other words, these changes could be biomarkers for disc infection. An important link in this developing chain is establishing whether Modic changes are associated with symptoms of LBP. Several studies evidence such an association [4, 5, 9–12] and provide prevalence estimates in LBP patients that vary widely, from 0.5 % [13] to 62 % [14] depending on study design, setting and inclusion criteria. A consensus seems to suggest that type 1 changes in particular are associated with symptoms of LBP [9–11, 15] and their prevalence in LBP patients ranges from 12 to 24 %. Based on this evidence, a randomised controlled trial (RCT) (162 participants) from Denmark investigated the effectiveness of antibiotics for hospital patients with severe chronic LBP with type 1 Modic changes [16]. It showed that co-amoxiclav (500/125 mg tablets, three times a day for 100 days) was better than placebo (effect size of 0.3 on RMDQ at end of 100 days of treatment and 1.0 at 12 months). The finding received much international attention. A replication RCT on 71 participants has since been published [17] and showed similar results. At least & Majid Artus m.artus@keele.ac.uk

Infection and low back pain: seeking evidence or fear of exploring new indications for antibiotics?