New data support an association between Chlamydia pneumoniae infection and multiple sclerosis (MS).
FaxWatch Inc.- June 4, 2001
“Although the etiology of MS is not known, indirect and circumstantial evidence suggests the role of an infectious agent in the disease process,” the study authors explained. “We chose to examine a possible link between chronic CNS infection with [C.] pneumoniae and MS because of our initial observation of CNS infection with C. pneumoniae in a patient with rapidly progressive MS.”
The researchers studied 17 patients with MS and 14 controls with other neurologic disease. In CSF samples, oligoclonal bands (representing intrathecal antibody synthesis) were evaluated for reactivity to C. pneumoniae antigens, measles, human heat shock protein-60, Escherichia coli, Staphylococcus aureus, and herpes simplex virus-1 antigens.
In 16 of the 17 MS patients, affinity-driven immunoblot studies showed reactivity of oligoclonal bands against elementary body antigens of C. pneumoniae. In contrast, none of the controls demonstrated a prominent reactivity to C. pneumoniae.
In 14 MS patients, oligoclonal bands were adsorbed partially or completely by antigens of C. pneumoniae. This was not seen with myelin basic protein, heat shock protein-60, or bacterial or viral antigens. In 3 controls with subacute sclerosing panencephalitis, oligoclonal bands were adsorbed with measles virus antigens but not antigens of C. pneumoniae.
“In virtually all infections of the CNS in which oligoclonal bands represent intrathecal antibody synthesis, the antigenic specificity of the immune response is directed against the infectious pathogen,” the authors concluded. “If this paradigm were to be extended to MS, it would indicate that C. pneumoniae, or an organism that is a close member of the C. pneumoniae family, may play a role in the immunopathology of CNS lesions in some patients with MS.” (Yao S-Y, et al. Neurology 2001;56:1168-76.)
In an editorial, Dr. Charlotte Gaydos urged readers “to exercise caution in their interpretation of these findings.” She noted that the evidence on an association between C. pneumoniae and MS is conflicting; using several different PCR methods to detect C. pneumoniae in CSF, her own group reported negative findings. Dr. Gaydos concluded, “More studies are needed to establish whether an association of C. pneumoniae with MS is ‘to be’ or ‘not to be’ confirmed by the scientific community.” (Neurology 2001;56:1126-7.)
Separately, Drs. Steven Jacobson and Anne Cross evaluated the evidence for an environmental cause of MS, specifically C. pneumoniae. As with Dr. Gaydos, they noted that technical limitations make it difficult to compare studies. “Ultimately, the test of any hypothesis on an infectious etiology in MS may have to rely on well controlled clinical trials of therapeutic agents specific for the proposed organism,” they wrote. “Until then … acceptance among the medical community will be circumspect.” (Neurology 2001;56:1128-9.)
Finally, Dr. Robert Griggs, editor-in-chief of Neurology, wrote, “For chlamydia and MS, more work is needed. ... A Multiple Sclerosis Society–funded, controlled clinical trial of the antibiotics rifampin and azithromycin that is in its inception stages may not give us the final answer as to whether there are [C.] pneumoniae in the CSF and brain of patients with MS, but it may tell us whether it matters.” (Neurology 20001;56:1130.)
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