Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Initiative
A Stanford initiative dedicated to studying infection-associated chronic diseases
3351 El Camino Real Suite 225
The ME/CFS Initiative conducts extensive clinical research in an effort to improve diagnosis and treatment of this debilitating illness. Stanford Medicine has had great success in engaging and collaborating with nearly 50 researchers across Stanford University and beyond. Together, they have discovered various potential biomarkers that have confirmed that ME/CFS is a real, physical disease. These discoveries are dramatically changing public and scientific opinions.
The ME/CFS team of dedicated physicians, nurse practitioners, nurses and researchers work jointly with patients, with the profound commitment to understanding the causes behind this debilitating disease and providing compassionate care and effective therapies to those affected by ME/CFS, and support to their families and caretakers.
Establish Stanford Program for Research and Treatment of Chronic Unexplained Illnesses
Programmatic goals would include conducting translational research, treating patients, and training the next generation of ME/CFS physician-scientists. Key aims of the program are:
- Identify biomarkers associated with chronic unexplained illnesses, including ME/CFS, with the aim of translating that knowledge into early diagnoses and effective treatments
- Become a clinical center of excellence for the diagnosis and treatment of patients with suspected or confirmed chronic unexplained illnesses, including ME/CFS
- Provide leadership and education in the field of infection-associated chronic unexplained illnesses
What is ME/CFS?
At Stanford, we believe that a subset of cases of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) may be related to infection. The nature of the association is still unknown, but we use two possible hypotheses in our research. One hypothesis is that the symptoms of ME/CFS could be triggered by the persistent activity of a pathogen (for example, a bacteria or virus) in the patient. However, the second hypothesis is that the symptoms of ME/CFS may be caused not by the pathogen itself, but rather by the body’s immune response to the pathogen.
Clinical, scientific and epidemiological observations made by several research groups, including our own, have led to the development of these hypotheses. From an epidemiological perspective, it has been known for many years that the onset of CFS is often acute and preceded by a viral or infection-like illness. Work led by Andrew Lloyd in Dubbo, Australia confirmed that the onset of CFS in some patients is marked by acute infection. Lloyd and his research team looked at acute infections of Epstein-Barr virus (glandular fever), Coxiella burnetii (Q fever), or Ross River virus (epidemic polyarthritis) in 253 patients. They found that six months after the acute infection, 11% of the patients developed CFS.1 This study demonstrates that in Australia, a number of patients developed CFS following an acute infection.
From the basic sciences point of view, it has been observed that many of the infectious agents that may be associated with ME/CFS remain in the body for the patient’s entire life (i.e, there is a latent infection). These infectious agents are usually obligate intracellular pathogens, meaning they can only survive by infecting a host cell. It is thus possible that the acute infection marking the onset of ME/CFS could become chronic and, in this manner, it could be biologically plausible that the infection could be responsible for a chronic illness.
It has also been observed that many infectious pathogens implicated in ME/CFS can affect the central nervous system. Cognitive impairment is a common feature of ME/CFS. It is possible that a chronic infection or inflammation in the brain may result in diminished cognitive capacity in these patients.
John Chia, MD, infectious disease specialist, has reported numerous findings that suggest an association between ME/CFS and infection with enteroviruses. It has been observed that ME/CFS patients commonly suffer from gastrointestinal complaints, and that between 35-92% of ME/CFS patients have irritable bowel syndrome2. Chia has observed, “80-90% of our 1400 ME/CFS patients have recurring gastrointestinal symptoms of varying severity… compared to only 3/100 controls.”3
In a recent study, Chia’s group found enterovirus VP1 protein in 82% of stomach biopsy samples of CFS patients, which “seems to correlate with the high percentage of CFS patients with GI complaints.” Additionally, “enteroviral protein was detected in the initial stomach biopsy specimens of six patients who developed GI infection before the onset of CFS, and also in biopsy specimens taken years later when the patients had persistent GI symptoms and fatigue.”3
“This finding suggests that enterovirus infection initiated GI symptoms and CFS, and the persistence of the virus years later likely was responsible for the patient’s symptoms.”3Chia’s clinical observations and research thus suggest a strong association between enteroviral persistence/infection and CFS.
Additionally, A. Martin Lerner, MD, president of the Treatment Center for ME/CFS, has reported in several publications that long-term antiviral treatment of a subgroup of CFS patients identified by different markers for herpesviruses have resulted in significant clinical improvement of their CFS related symptoms.4
In summary, it is plausible that the persistent activity of intracellular pathogens or the immune response against them could lead to the complex and chronic dysfunction observed in patients with ME/CFS. Furthermore, it is possible that if the infectious trigger is appropriately identified, significant clinical benefit can be observed with appropriate long-term antimicrobial therapy.
1 Hickie et al. “Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study.” BMJ. 2006 Sep 16;333(7568):575. Epub 2006 Sep 1.
2 Frissora CL, Koch KL. “Symptom overlap and comorbidity of irritable bowel syndrome with other conditions.” Curr Gastroenterol Rep. 2005 Aug;7(4):264-71.
4 Lerner AM et al. “Subset-directed antiviral treatment of 142 herpesvirus patients with chronic fatigue syndrome.” Virus Adaptation and Treatment May 2010:2 47-57