Intracellular infections:
As discussed previously, there seems to be an assumption that there is only one causative agent for every disease, and the focus in MS is on some as-yet unexplained autoimmune response. Yet most authorities agree that there is a genetic basis to MS but that the contribution of genes is small, and the contribution of unexplained environmental factors is the larger factor in who will get MS and how the disease will progress. This well-established position does not sit well with the neat autoimmune theory. Even those who subscribe to the autoimmune theory cannot be certain of whether it arises inside the CNS or outside of it. http://multiple-sclerosis-research.blogspot.com/2012/07/will-real-ms-please-stand-up.html
Others have raised considerable doubts about the validity of the autoimmune theory. http://www.direct-ms.org/pdf/ImmunologyMS/MS_Not_Autoimmune.pdf and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361990/
Yet billions of dollars are invested in and spent on drug therapies that are based on this theory, exposing thousands of people to severe side effects, ranging from the merely inconvenient, to death.
Similarly, when an infectious cause for MS is being sought, there seems to be a tremendous focus on looking for a single causative organism. Unsurprisingly, no single causative organism has ever been found, and MS is not a contagious illness, despite efforts to see if it can be passed from one individual to another.
Perhaps one part of the answer is this: Insofar as an infectious cause is at play in some susceptible individuals, it may not matter which organism the individual is infected with, whether it be a virus, bacterium, amoeba or whatever, discovered or as yet undiscovered, so long as the organism persists in the body after infection, and provokes a particular response by the body which creates the damaging physiological responses to the infection that are characteristic of MS.
Several intracellular infections have been linked to MS, and it appears that there are several ways in which they may affect the disease process, primarily:
The assumption in textbooks and research documents seems to be that everything in MS is driven by damage in the CNS, and there is a kind of progressive paralysis arising from this damage. This may well be the case, but this mechanism is not definitively explained, and it is postulated presumably by people who do not live with, or experience the disease. People with progressive MS do experience a creeping paralysis, but it often does not feel like a straightforward CNS injury. They can complain of a fatigue that is devastating and often precedes any visible lesions in the CNS, sometimes by years, and which can catastrophically worsen without any visible changes to existing lesions in the CNS.
There is often severe muscle pain and although the limbs can be moved, there is ‘nothing in the tank’ to move them with. Sometimes there is plenty in the tank to start with, but the tank starts emptying at progressively shorter intervals. When a person with MS turns to the scientific literature for an explanation of this crushing fatigue, they may find a weak and unproven theory about ‘slowed nerve transmission’ that does not explain the fact that they may feel very ill, with symptoms more reminiscent of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome, and that they look drawn and ill, and feel sick all the time, like they have a severe case of the flu. http://www.rickettsialab.org.au/#!__page-7
Note: When we get the flu, we can be bedridden in a matter of hours, with fever or chills, headache, wracked with terrible muscle pain, dizzy, unable to think clearly, and our limbs feel like lead. If we have to get up, we can barely move. We just want to withdraw from social contact and lie down somewhere quietly. We look, feel and act depressed. These effects are called sickness behaviours and are not necessarily a direct result of the action of the flu virus, but the body’s ‘red alert’ immune system response to the viral attack. Is it possible that those of us with progressive MS who continue to manifest these sickness behaviours in our disease course; muscle aches, social withdrawal, brain fog, depression, low grade fever or chills, and weak, heavy limbs, and physical crashes requiring bedrest are demonstrating an underlying low grade infection, or at least an immune system that considers it is suffering a continual low grade infection?
As noted above, there are some diseases which mimic MS precisely. One of these is Syphilis, and although some may find this insulting or confronting, a neurologist should eliminate Syphilis as a differential diagnosis in MS. If Syphilis produces identical symptoms to MS it is hardly a stretch to accept that there are other disease processes that could create the same result.
Another obvious one is Lyme Disease and its co-infections. Lyme Disease is caused by a spirochete, as is Syphilis, but Lyme Disease is a tick borne infection with a disease process that can mimic MS precisely, including lesions on MRI. However, the concept which is being laid out for consideration here is that the process may be subtler and more complex than a directly causative disease agent, and that potentially in MS it is not the type of infection that matters, but only that the immune response remains switched on, whether it is appropriate or not, and it is this constant immune engagement that is part of the complex interplay of factors that creates the symptomology of progression.
If there is an infection of one type or another at work in progressive MS, it is clearly not one that overpowers the patient in one devastating attack. It is more like a slow overwhelming of a person’s resources, the rate of which varies between one individual and another.
It is not true that if we are not killed by an infection, we are cured of it. For example; The painful sores of Shingles are caused by a virus called varicella-zoster. Its common name is chickenpox. If you suffer from a bout of chickenpox, then when you recover, the symptoms go away, but the virus remains with you for life, hiding out in nerve cells, most usually in the spine. Then sometimes the virus reactivates, follows a nerve path, and surfaces at the nerve ends on the skin, causing painful blisters.
This is an acute reactivation, and many people are seriously affected and need medical assistance to get over it. This pattern of fighting off Shingles and then experiencing further bouts can recur several times. This is not to suggest that Shingles causes MS, only to demonstrate that infective agents can persist in ways that could account for benign MS, relapsing remitting MS and progressive MS, depending on individual immune responses. In the case of progressive MS, it may be that there is a more chronic infection that is typified by a period of ‘trench warfare’ where neither side gains the upper hand and the body just keeps the ‘army’ on constant alert, catabolising muscle until it can no longer fund the campaign, and runs out of ammunition, leaving a body without any capacity to ‘fund’ normal activities.
The concept is that in MS, more than one causal factor can be at work, in different individuals and even within the same individual, causing complex interrelated effects. An overlay of different factors that on their own may not amount to much, but together may create a perfect storm. Not so much ‘MS’, but an ‘MS Complex’. Infection may be a key part of this puzzle.
Lyme Disease and Co - Infections
As discussed previously, there seems to be an assumption that there is only one causative agent for every disease, and the focus in MS is on some as-yet unexplained autoimmune response. Yet most authorities agree that there is a genetic basis to MS but that the contribution of genes is small, and the contribution of unexplained environmental factors is the larger factor in who will get MS and how the disease will progress. This well-established position does not sit well with the neat autoimmune theory. Even those who subscribe to the autoimmune theory cannot be certain of whether it arises inside the CNS or outside of it. http://multiple-sclerosis-research.blogspot.com/2012/07/will-real-ms-please-stand-up.html
Others have raised considerable doubts about the validity of the autoimmune theory. http://www.direct-ms.org/pdf/ImmunologyMS/MS_Not_Autoimmune.pdf and http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361990/
Yet billions of dollars are invested in and spent on drug therapies that are based on this theory, exposing thousands of people to severe side effects, ranging from the merely inconvenient, to death.
Similarly, when an infectious cause for MS is being sought, there seems to be a tremendous focus on looking for a single causative organism. Unsurprisingly, no single causative organism has ever been found, and MS is not a contagious illness, despite efforts to see if it can be passed from one individual to another.
Perhaps one part of the answer is this: Insofar as an infectious cause is at play in some susceptible individuals, it may not matter which organism the individual is infected with, whether it be a virus, bacterium, amoeba or whatever, discovered or as yet undiscovered, so long as the organism persists in the body after infection, and provokes a particular response by the body which creates the damaging physiological responses to the infection that are characteristic of MS.
Several intracellular infections have been linked to MS, and it appears that there are several ways in which they may affect the disease process, primarily:
- The unique effect the individual organism has on the patient by the way it infects and attacks particular sites in the body, such as the nervous system
- The toxic by-products the organism may produce at different sites in the body, but particularly the CNS
- The commandeering of nutrients and energy production by the invaders at the expense of the host
- The way in which intracellular organisms evade detection by the immune systems, creating direct collateral damage (e.g. biofilms clogging arteries to the brain)
- The way in which intracellular organisms evade detection by the immune systems, potentially provoking autoimmune reactions in various ways
- The way in which intracellular organisms can persist, creating an immune war that never ends, flooding the body with inflammatory chemicals, provoking devastating symptoms of ‘sickness behaviours’ and ultimately depleting the body of the proteins it needs (antibodies or immunoglobulins) to fight the battle. In these conditions where the body goes into survival mode and starts catabolising muscle to fight the never ending war against the invader, the body begins to run out of ammunition and may enter a state of progressively worsening exhaustion that is seen in progressive MS.
The assumption in textbooks and research documents seems to be that everything in MS is driven by damage in the CNS, and there is a kind of progressive paralysis arising from this damage. This may well be the case, but this mechanism is not definitively explained, and it is postulated presumably by people who do not live with, or experience the disease. People with progressive MS do experience a creeping paralysis, but it often does not feel like a straightforward CNS injury. They can complain of a fatigue that is devastating and often precedes any visible lesions in the CNS, sometimes by years, and which can catastrophically worsen without any visible changes to existing lesions in the CNS.
There is often severe muscle pain and although the limbs can be moved, there is ‘nothing in the tank’ to move them with. Sometimes there is plenty in the tank to start with, but the tank starts emptying at progressively shorter intervals. When a person with MS turns to the scientific literature for an explanation of this crushing fatigue, they may find a weak and unproven theory about ‘slowed nerve transmission’ that does not explain the fact that they may feel very ill, with symptoms more reminiscent of Myalgic Encephalomyelitis or Chronic Fatigue Syndrome, and that they look drawn and ill, and feel sick all the time, like they have a severe case of the flu. http://www.rickettsialab.org.au/#!__page-7
Note: When we get the flu, we can be bedridden in a matter of hours, with fever or chills, headache, wracked with terrible muscle pain, dizzy, unable to think clearly, and our limbs feel like lead. If we have to get up, we can barely move. We just want to withdraw from social contact and lie down somewhere quietly. We look, feel and act depressed. These effects are called sickness behaviours and are not necessarily a direct result of the action of the flu virus, but the body’s ‘red alert’ immune system response to the viral attack. Is it possible that those of us with progressive MS who continue to manifest these sickness behaviours in our disease course; muscle aches, social withdrawal, brain fog, depression, low grade fever or chills, and weak, heavy limbs, and physical crashes requiring bedrest are demonstrating an underlying low grade infection, or at least an immune system that considers it is suffering a continual low grade infection?
As noted above, there are some diseases which mimic MS precisely. One of these is Syphilis, and although some may find this insulting or confronting, a neurologist should eliminate Syphilis as a differential diagnosis in MS. If Syphilis produces identical symptoms to MS it is hardly a stretch to accept that there are other disease processes that could create the same result.
Another obvious one is Lyme Disease and its co-infections. Lyme Disease is caused by a spirochete, as is Syphilis, but Lyme Disease is a tick borne infection with a disease process that can mimic MS precisely, including lesions on MRI. However, the concept which is being laid out for consideration here is that the process may be subtler and more complex than a directly causative disease agent, and that potentially in MS it is not the type of infection that matters, but only that the immune response remains switched on, whether it is appropriate or not, and it is this constant immune engagement that is part of the complex interplay of factors that creates the symptomology of progression.
If there is an infection of one type or another at work in progressive MS, it is clearly not one that overpowers the patient in one devastating attack. It is more like a slow overwhelming of a person’s resources, the rate of which varies between one individual and another.
It is not true that if we are not killed by an infection, we are cured of it. For example; The painful sores of Shingles are caused by a virus called varicella-zoster. Its common name is chickenpox. If you suffer from a bout of chickenpox, then when you recover, the symptoms go away, but the virus remains with you for life, hiding out in nerve cells, most usually in the spine. Then sometimes the virus reactivates, follows a nerve path, and surfaces at the nerve ends on the skin, causing painful blisters.
This is an acute reactivation, and many people are seriously affected and need medical assistance to get over it. This pattern of fighting off Shingles and then experiencing further bouts can recur several times. This is not to suggest that Shingles causes MS, only to demonstrate that infective agents can persist in ways that could account for benign MS, relapsing remitting MS and progressive MS, depending on individual immune responses. In the case of progressive MS, it may be that there is a more chronic infection that is typified by a period of ‘trench warfare’ where neither side gains the upper hand and the body just keeps the ‘army’ on constant alert, catabolising muscle until it can no longer fund the campaign, and runs out of ammunition, leaving a body without any capacity to ‘fund’ normal activities.
The concept is that in MS, more than one causal factor can be at work, in different individuals and even within the same individual, causing complex interrelated effects. An overlay of different factors that on their own may not amount to much, but together may create a perfect storm. Not so much ‘MS’, but an ‘MS Complex’. Infection may be a key part of this puzzle.
Lyme Disease and Co - Infections