David Wheldon and Dr A were asked about the reason that steroids and immunosuppressants do not cause CPN to go out of control in the case of MS. If people with MS actually have CPn, why are steroids or things like tysabri apparently helpful? Why do they not make people worse? answer follows:
DR A's response (the MD who is close to the VU work who is expert)
As far as steroids are concerned, the cellular immune system isnâ€™t very effective against C. pneumoniae infections (The C. pneumoniae can infect every cell in the cellular immune system.). Therefore, interfering with the cellular immune system ( by giving something like steroids or suppression of the immune system ed.) would be predicted to have little to do with making the disease worse â€“ and might make the symptoms better if the symptoms were related to inflammation.
If inflammation is the only effective host response against C. pneumoniae, interfering with the inflammatory response might actually make the symptoms better, but could make the disease worse. Consider what Cox-2 inhibitors might be doing to athersclerosis in this context.(this is in reference to the fact that CPn is implicated in atherosclerosis and that medication like Vioxx is shown to increase incidence of heart problems ed.)
It may be that the more effective the anti-inflammatory effect, the more â€œout of controlâ€? the C. pneumoniae infection may be â€“ but this needs to be determined scientifically. Chlamydial infections, in general, are not serious, although serious infections by this pathogen have been described. See abstract below.
Scand J Infect Dis. 1998;30(5):523-4.
Chlamydia pneumoniae infection associated with multi-organ failure and fatal outcome in a previously healthy patient.
Gnarpe J, Gnarpe H, Nissen K, Haldar K, Naas J.
Department of Clinical Microbiology, Gavle Central Hospital, Sweden.
Chlamydia pneumoniae has been associated with respiratory infections and with cardiovascular disease. We describe here a patient with multi-organ failure and fatal outcome in whom C. pneumoniae was implicated as a causative agent. Serological analysis for C. pneumoniae was done by immunofluorescence. Immunohistochemistry was carried out with avidin-biotin peroxidase staining. The patient had pneumonia I month prior to death. C. pneumoniae was detected in the heart and lungs by immunohistochemistry at autopsy. The patient had an antibody pattern suggestive of current or chronic C. pneumoniae infection. Serological analysis for Legionella sp., Mycoplasma pneumoniae, CMV, EBV, enteroviral agents and markers for autoimmune disease were negative. The findings suggest C. pneumoniae as the aetiological agent in this case of multi-organ failure.
DR WHELDON'S RESPONSE
My guess is that this is a very slow infection, and, if you consider Alzheimer's disease, may take 50 or more years to develop symptomatically. When it goes into the cryptic form it replicates very slowly indeed. Nevertheless it may provoke a massive cellular reaction, particularly after a new respiratory infection. Steroids to cover these acute phases would seem reasonable.
Why doesn't the infection get out of control when Natalizumab is used? Well, it's early days yet. Let's see what happens in 10 or fifteen years.