For all the skeptical glances some chiropractors may cast upon infectious agents and antibiotics come a brace of papers that tell us in no uncertain terms that, in the final analysis, chiropractors need to respect the pathogen.
First up is a study of 162 patients whose only known illness was chronic low back pain lasting more than six months following a previous disc herniation, and who also had bone edema (Modic type 1) changes in the vertebra adjacent to the previous herniation. This investigation was sparked by two previous observations: (1) Bacteria were found in no less than 37 percent of patients with disc herniation, not in those without the disc disorder; and (2) Modic type I changes or bone edema in the vertebra were present in about the same proportion of those with low back pain. This matches the observation of investigators at the University of Southern Denmark, who found that 20-40 percent of chronic lower back pain was caused by bacterial infections.
All patients were randomized to 100 days of antibiotic treatment (Bioclavid) or a placebo and were evaluated at baseline, the end of treatment and at one year of follow-up, at which point 144 patients still remained in the study. The primary (disease-specific disability and lumbar pain) and secondary (leg pain, number of hours of pain lasting four weeks, global perceived health, days with sick leave, bothersomeness, constant pain, and MRI) outcomes all displayed a greater response to the antibiotic than to the placebo.
The cost of this lengthy course of antibiotics was just 114 British pounds. One would have to suspect from this study that the investigators may have come across a previously unrecognized cause of chronic back pain and an effective treatment in a subgroup of patients.1 This finding, of course, awaits confirmation at additional sites.
Why belabor this point about the bacteria? Simply because elsewhere, in the hot-button domain of the safety of spinal manipulation, no less, there remains a persistent, unsolved and ultimately troubling series of investigations beginning in the middle 1990s that have linked acute cerebrovascular ischemia and chronic and recurrent infection.
A case-control study in 1995 of 197 patients revealed that respiratory infections increased the risk of ischemia in all age groups and reached significance in patients ages 51-70. The profile of vascular risk factors was similar in patients with or without previous infection. Previous stroke, hypertension, diabetes mellitus, coronary heart disease, and current smoking simply raised the probability of infection being a significant risk factor.2
The same group of investigators (in the same year) found that, in patients with a recent infection, the neurological deficit on admission was more severe, cortical infarcts in the middle cerebral artery territory were more frequent, the prevalence of extracranial stenoses was actually lower, and definite or presumed cardioembolic stroke was more frequent – as was stroke from cervical artery dissections. Serum levels of C-reactive protein were more than twice as high in patients carrying infections.3
To complete their trifecta, Grau's group focused upon chronic or recurrent respiratory, ear-nose-throat and dental infections. Matching 166 patients with acute cerebrovascular ischemia against an equal number lacking this condition, the investigators found that two or more episodes of chronic bronchitis in each of the two preceding years was associated with stroke in age-adjusted multiple logistic regression analyses. Stroke patients also tended to have poorer dental status, mainly resulting from a chronic dental infection – which itself was classified as a stroke risk factor.4
Focusing upon particular pathogenic species, two separate case-control studies were able to demonstrate that chronic Heliobacter pylori infection was associated with a higher risk of stroke caused by small-artery occlusion, but a lower risk of cardioembolic stroke.5-7 At the same time, elevated antibodies to H. pylori, as well as Chlamydia pneumoniae, were not associated with stroke;5 but a later case-control study did support the association of an immune response with stroke.6
A later study involving lipoprotein-associated lipoprotein phospholipase, which mediates inflammation in atherosclerosis, suggested that C. pneumoniae does play an interactive role in accelerated inflammation in atherlosclerosis.8
What does all this mean? Simply that, along with the role of inflammation, which has become more recognized across the health professions as a major risk factor, the role of bacterial infection needs to be acknowledged as highly significant and most likely a prelude to many instances of inflammation.
Just as chiropractors should have a strong background in pharmacology (since many of their patients will most likely be taking or have taken medication), so should they take heed and pay regard to the unavoidable fact that their patients are bringing in all manner of baggage – including bacterial pathogens. Simply put: Louis Pasteur lives.
References
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