Because it has been such a prominent part of my own illness, I've done quite a bit of research on porphyria. Almost everything in the literature refers to primary genetic porphyria, though there are a few references to secondary (non-genetic) porphyria caused by various liver-destroying processes.
Primary porphyria is a genetic disease in which there is a deficiency of one of eight different enzymes, each of which is required to effect one of the eight sequential steps required to synthesis the iron-containing protein heme. The output at each step is the precursor for the next step of heme synthesis. A deficiency of one of the enzymes can cause accumulation of the precursor from the previous step and prevent the subsequent steps from producing heme.
Normally, finished heme output feeds back to the first of the eight steps, and halts heme production when sufficient heme has been synthesized.
In primary genetic porphyria, heme production is compromised, and thus sufficient finished heme feedback doesn't occur to halt the continued attempt to make heme, and one of the precursors continues to accumulate.
These precursors, called porphyrins, are highly neurotoxic, though normally they exist only transiently in the heme manufacturing pipeline. In primary genetic prophryia, not all porphyrins are converted to heme and accumulate to excess. When accumulated to sufficient levels, these porphyrins trigger the various manefestations of the various forms of porphyria.
Primary genetic porphyria attacks are triggered when the body is called upon to make an amount of heme that exceeds the limit imposed by the insufficient enzyme level. Most porphyriacs can make sufficient heme for ordinary activities, but are unable to make larger amounts of heme required for exceptional circumstances.
Thus, porphyria is an episodic illness that occurs when the body is occasionally called upon to make more heme than can be produced by the compromised heme-making machinery.
While all cells manufacture some amount of heme, the greatest amount of heme is manufactured during the production of red blood cells. Most of the rest of the body's heme is manufactured by the liver. However, red blood cell production is a relatively steady-state operation, and would thus not be expected to be involved in requirments to make exceptional amounts of heme, and would thus not be expected to be involved in porphyria attacks.
The liver, on the other hand, is involved in large numbers of processes that are anything but steady state. An examination of classical porphyria triggers such as alcohol consumption, tobacco consumption, intense exercise, illicit and licit drug consumption, and dietary changes show that these are all environmental factors that heavily impinge upon liver function.
Fundamentally, then, primary genetic porphyria is a disease of the liver.
Switching gears a bit now, Stratton has indicated that Cpn infection causes a disruption of heme manufacture via mitchondrial dysfunction. The pipe-lined steps of heme manufacture are disrupted due to lack of ATP either inside or outside of the mitochondria due to ATP-theft by Cpn, rather than due to enzyme insufficieny. However, the end result is the same as in primary genetic porphyria, namely accumulation of pophyrins.
Thus, Cpn infection could be expected to produce acute porphyria attacks that mimic the accute attacks seen in primary genetic porphyria, and such Cpn-mediated attacks could be expected to be triggered by classical primary genetic porphyria triggers.
However, Cpn infection also seems capable of interfering with even normo-intensive heme manufacture, and thus can produce background level of porphyrins, even when classical triggers don't exist.
Furthermore, when Cpn-infected host cells lyse as a consequence of Cpn RB destruction via antibiotics, accumulated intracellular porphyrins are released into the blood stream.
Thus, Cpn infection produces three distinct porphyria phenomena:
1. Acute porphyria attacks similar in nature to primary genetic porphyria and which are triggered by classical primary genetic porphyria triggers that induce calls for exceptional amounts of heme. Such Cpn-mediated attacks would be expected to produce elevated porhyrin levels similar to elevations seen in primary genetic porphyria acute attacks.
2. Interference with normo-intensive heme production, resulting in slightly and chronically elevated porphyrin levels at all times.
3. Pulsed releases of relatively larger amounts of porphyrins than seen in Item 2 above during host cell apoptosis as a consequence of RB destruction due to antibiotic treatment, with such amounts related to the degree of preceding RB destruction.
Finally, based upon the earlier explanation of primary genetic porhyria being fundamentally a disease of the liver, and leaving aside the possibiity of erythroid Cpn infection, I'm going to assert that essentially ALL clinical porphyria phenomena seen in Cpn infection are a function of Cpn infection of the liver specifically. Thus the degree of Cpn liver infection is going to influence the degree of the three Cpn porphyria phenomena.
This explanation would account for the different degrees of difficulty experienced by those undergoing CAP treatment for Cpn infection. In particular, this may explain why many of those with MS (and perhaps certain other Cpn-caused conditions) do not experience the three Cpn porphyria phenomena, whereas those with CFS/CFID/MCS/GWS usually do. That is, people who experience porphyria symptoms have a Cpn liver infection, and those that do not experience porphyria symptoms don't have a Cpn liver infection.
Most people with CFS/CFID/MCS/GWS/ME most likely have Cpn liver infections since most of these people report porphyria symptoms. Those people with MS and other conditions who do not report porphyria symptoms most likely do not have a concurrent Cpn liver infection.