Chronic Fatigue Syndrome (CFS) or Myalgic Encephalomyelitis (ME). Considerations of its infectious etiology
The chronic fatigue syndrome (CFS: Chronic Fatigue Syndrome) or myalgic encephalomyelitis (ME: Myalgic encephalomyelitis), is a complex disease without debilitating curative, whose etiology is unknown. Patients affected by this syndrome show a significant loss of physical and mental functional activity, leading to dependence on wheelchairs, stay at home and even in bed. The main symptoms are discomfort and worsening of symptoms after minimal physical or mental effort that persist for hours, days or weeks, who do not improve with rest or sleep. Other symptoms include chronic fatigue, cognitive impairment, non - restorative sleep, pain and a host of neurological symptoms. The disease has a prolonged over years with remissions and recurrences course. It is an endemic syndrome with sporadic cases and occasional outbreaks of grouped cases, affecting all races and age groups. There is no specific diagnostic test for this syndrome so the diagnosis is clinical using various case definitions which define the pattern of diagnostic symptoms, which requires the exclusion of other diseases with similar manifestations by clinical history, physical examination and additional tests .
There is controversy about whether it is organic disease or psychological disorder and sometimes even the existence of CFS / ME refuses as a disease. As for its causes it has been considered a psychosomatic disorder, some infectious agents, immune dysfunction, an autoimmune process, some metabolic disorders, the effects of toxins or inherited genetic factors. Clinical, immunological and epidemiological evidence supports the hypothesis that it is an infectious disease whose causative agent in patients persist; the pathogen should be transmitted by contact or bite of a vector; host factors that determine host susceptibility to disease; that there is a population of healthy carriers can eliminate the pathogen; which it is endemic to sporadic cases and occasional outbreaks of clustered cases. The existence of clustered cases supports the involvement of an infectious agent, which would result in outbreaks of cases and often sporadic flu - like beginning. Infectiousness is based on the existence of secondary cases in outbreaks, most prevalent in sporadic cases in close contacts in the rest of the community. The chronicity of symptoms and immunological changes, and the existence of secondary cases suggest the persistence of the causative pathogen in patient suffering. Considered risk factors that predispose to CFS / ME are familiar next member with CFS / ME; female; previous infectious diseases; and occupational exposure of healthcare professionals. However, it has not proved the existence of a known pathogen and continue currently investigating the implication of unknown or known pathogens. Currently, several renowned organizations such as the CDC (Center for Disease Control US), not included in the definition of case the involvement of any infectious agent or perform any diagnostic adjunctive test to help diagnose . In the same way, nor include defnitions case "Clinical Canadian ME / CFS definition" (2003) nor the "International Consensus Criteria for myalgic encephalomyelitis -by" (2011).
Involvement of infectious agents in the syndrome
Currently it is considered that there is no cause of CFS / ME known pathogen and the possible association of some known pathogens and CFS / ME is complex. Some known pathogens may contribute to the onset of the disease and the severity of symptoms. They have been linked to several infectious diseases in 6 months to 2 years before the start that could trigger it . In outbreaks of cases they have been conducted bacteriological and virological studies and the search for antibodies against them and the evidence found in some cases contradictory in others. In general, the only thing achieved sometimes is greater prevalence of antibodies to a particular agent, regarding a group of control individuals. At other times it has achieved a favorable response with some antimicrobial, antiviral or administration of intravenous immunoglobulins.
Sometimes, all that has been achieved is to relate similar symptoms that occurs in some infections chronic type, with the typical manifestations of CFS / ME. This has motivated the search for these infections in cases of CFS / ME, but no such agent has been admitted as the cause of the syndrome. This is what happened when the neurological forms of Lyme disease caused by Borrelia burgdorferi were described.
Some studies have also investigated the possible effect of coinfection, as has happened with Chlamydophila pneumoniae, Mycoplasma spp. and human herpes virus type 6 (HHV6).
On other occasions found antibodies that cross - react with known agents (eg. Poliovirus) has made think of a related virus that could not be isolated from patients. Similarly it has happened with retrovirus related to HTLV-2 virus or XMRV.
In some cases grouped outbreaks, the blood of patients was inoculated monkeys and could be transmitted from monkeys to others, observed in the histopathological study the existence of infiltrates of lymphocytes and mononuclear cells damage the myelin sheath and swelling of the axon. Inoculation of monkeys with blood from patients from other outbreaks cases showed perivascular cuffing of blood vessels root of dorsal root ganglia, roots and lumbar nerves cervical, brain and spinal cord of monkeys inoculated.
They were considered large number of viral pathogens, bacterial or protozoa sometimes initiated syndrome CFS / ME so it has been speculated that it could be the clinical outcome of the infection of a host by various microorganisms, whose hypothesis would lead to these agents cause CFS / ME infecting the vagus nerve and the symptoms and the process would be an exaggerated response with release of cytokines that affect the brain when vagal sensory ganglia or paraganglia became infected with any pathogen. The difficulty in finding a causal agent may be related to the phenomenon of latency that could lead to localized immune response in infected nerve ganglia. It may also occur that the infectious agent and then initiate the process disappear after the onset of symptoms resulting immune dysfunction and / or autoimmunity (theory "hit and run"). However, this theory contradicts the existence of secondary cases in the affected contacts during some outbreaks of clustered cases. The continued existence of immune mechanisms suggests that the agent must persist.
Ratio considered infectious agents
- Borrelia burgdorferi (Lyme disease).
- Chlamydophila pneumoniae.
- Mycoplasma spp.
- Rickettsia spp. (fevers group soiled with different species depending on location).
- Coxiella burnetii (Q fever and chronic cases of syndromes postQ).
- Leptospira interrogans with different serovars.
- Herpes simplex virus types 1 or 2 (HHV-1, HHV-2)
- Herpes simplex virus type 6 (HHV-6).
- Epstein-Barr virus (EBV).
- Coxsackie B virus types 1 to 6) (B Enterovirus).
- Parvovirus B19 (B19 Erythrovirus).
- Rubella virus.
- Hepatitis viruses.
- Tick - borne encephalitis virus.
- Babesia microti.
- Chronic exposure to fungi.
- Exposure to biotoxins.
Microbiological tests recommended
There is no recommended to diagnose this syndrome microbiological testing. Microbiological tests that have been conducted have sought the involvement of an infectious agent in the syndrome.
Furthermore, testing for the presence of a pathogen, to exclude that it is a proper process of chronic or latent phase of infection by a particular infectious agent, for if found excluded that the case CFS / ME, while using an antimicrobial / antiviral therapy in case there is for the treatment of this infectious process.
Tests in IVAMI
- Any test that can be applied to rule out infection by the agents mentioned. In most cases the antibody research is recommended as it would be past, persistent or latent infections, which may be absent genome of the organism in peripheral blood.