Myalgic encephalomyelitis

Comment on: Myalgic encephalomyelitis. [J R Soc Med. 1991]

 

The exchange of views between Drs Wessely and Wilson in the correspondence columns of the March issue of the Journal (March 1991 JRSM, p 182) highlights the divergence of opinion concerning the nature of myalgic encephalomyelitis (ME).

Recognition of ME as a significant health problem in New Zealand dates from an outbreak of ‘Tapanui ‘flu’ in a small country town in 1983. As it seemed possible that the wide range of symptoms could be indicative of impaired capillary blood flow, we studied the filtrability of blood samples from members of ME support groups. We found that subjects who were acutely unwell had prolonged blood filtration times which returned towards normal in the chronic state.

More recently it has been shown that ME symptoms are associated with increased percentages of nondiscocytic erythrocytes and the percentage of such cells showed an inverse correlation with wellbeing. The significance of altered red cell shape in the pathogenesis of ME has been discussed and it has been found that an injection of vitamin B12 improved wellbeing within 24 h. The loss of symptoms was associated with reduced percentages of nondiscocytes in about 50% of subjects. Those who failed to perceive a beneficial response from the B12 showed no change in red cell shape. Further studies at varying degrees of completion confirm and extend the published observations.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1295578/pdf/jrsocmed00119-0075a.pdf

 

Source: Simpson LO. Myalgic encephalomyelitis. J R Soc Med. 1991 Oct;84(10):633. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1295578/

 

Immunology of postviral fatigue syndrome

Abstract:

Postviral fatigue syndrome is associated with persistent infection by a virus. The patient with the condition has failed to eliminate the virus in the usual time. There is little evidence of a deficient immune response by the patient as the explanation for the viral persistence, and it must be assumed that most of the explanation lies in down-regulation of virus expression in infected cells. The general symptomatology of postinfectious syndromes may be mediated by cytokines liberated as part of the infection. Part of the syndrome may also be due to local effects of virus infection in muscles or the central nervous system (CNS).

 

Source: Mowbray JF, Yousef GE. Immunology of postviral fatigue syndrome. Br Med Bull. 1991 Oct;47(4):886-94. http://www.ncbi.nlm.nih.gov/pubmed/1724405

 

Amplification and identification of enteroviral sequences in the postviral fatigue syndrome

Abstract:

Evidence from several sources has long suggested that enteroviruses might play a role in the postviral fatigue syndrome (PVFS).

We used the most sensitive molecular virological method available at present, the polymerase chain reaction (PCR) amplification technique, to look for enteroviral copies in peripheral blood leucocytes and muscle from a well-defined group of patients. We demonstrated that our PCR method amplified a sequence common to a wide range of enteroviral serotypes. A highly significant number of the muscle biopsies (53%: P = less than 0.001) from the patients were positive for enteroviral sequences. With regard to the leucocyte samples, 16% in both patient and control were positive.

The PCR results on the peripheral blood leucocytes were in keeping with serological findings, in showing that the level of exposure to enteroviruses seemed to be the same in patients and controls: it was therefore of the greatest interest that patients were 6.7 times more likely to have enteroviral genome in their muscle.

We conclude that persistent enteroviral infection plays a role in the pathogenesis of PVFS, also providing preliminary evidence that severe mitochondrial injury is one of the mechanisms involved.

 

Source: Gow JW, Behan WM. Amplification and identification of enteroviral sequences in the postviral fatigue syndrome. Br Med Bull. 1991 Oct;47(4):872-85. http://www.ncbi.nlm.nih.gov/pubmed/1665380

 

Persistent virus infection of muscle in postviral fatigue syndrome

Abstract:

Nucleic acid was extracted from muscle biopsy samples from a series of highly selected patients suffering from chronic muscle fatiguability following a viral infection (Postviral Fatigue Syndrome: PVFS).

Samples were examined for the presence of enteroviral RNA sequences or Epstein-Barr (EBV) virus DNA sequences by molecular hybridisation as these two agents have been implicated by retrospective serology in the aetiology of PVFS. We found enteroviral RNA in 24% of biopsy samples and EBV DNA in a further 9% of biopsy samples: no biopsy was positive for both enteroviral RNA and EBV DNA.

In addition, in the case of enteroviruses we found that the persisting virus is defective in control of RNA replication as both strands of enteroviral RNA are present in similar amounts: this is unlike the asymmetric synthesis of genomic RNA seen in a productive, cytolytic enterovirus infection. The implications of these data in relation to mechanisms of viral persistence and muscle dysfunction are discussed.

 

Source: Cunningham L, Bowles NE, Archard LC. Persistent virus infection of muscle in postviral fatigue syndrome. Br Med Bull. 1991 Oct;47(4):852-71. http://www.ncbi.nlm.nih.gov/pubmed/1665379

 

Fibromyalgia and parvovirus infection

Abstract:

An infectious cause of fibromyalgia (FM) has been hypothesized based upon the observed similarity of this entity and chronic fatigue syndrome. Three patients developed symptoms of FM after documented episodes of acute parvovirus B19 infections. B19 antibody determinations were obtained approximately 1 month after the symptoms began; both IgM and IgG titers were positive at that time. All 3 patients met criteria for FM. Polysomnography performed on 2 of the patients revealed profound alpha-wave intrusion throughout nonrapid eye movement sleep. A more careful search for viral infections in FM patients whose symptoms appear following a “flu-like” illness appears warranted.

 

Source: Leventhal LJ, Naides SJ, Freundlich B. Fibromyalgia and parvovirus infection. Arthritis Rheum. 1991 Oct;34(10):1319-24. http://www.ncbi.nlm.nih.gov/pubmed/1657005

 

Genomic polymorphism, growth properties, and immunologic variations in human herpesvirus-6 isolates

Abstract:

Fifteen human herpesvirus-6 (HHV-6) isolates from normal donors and patients with AIDS, systemic lupus erythematosis, chronic fatigue syndrome, collagen-vascular disease, leukopenia, bone marrow transplants, Exanthem subitum (roseola), and atypical polyclonal lymphoproliferation were studied for their tropism to fresh human cord blood mononuclear cells, growth in continuous T cell lines, reactivity to monoclonal antibodies, and by restriction enzyme banding patterns. All isolates replicated efficiently in human cord blood mononuclear cells, but mitogen stimulation of the cells prior to infection was required. The ability to infect continuous T-cell lines varied with the isolates. Isolates similar to GS prototype infected HSB2 and Sup T1 cells and did not infect Molt-3 cells, whereas isolates similar to Z-29 infected Molt-3 cells but not HSB2 and Sup T1 cells. Some of the monoclonal antibodies directed against the HHV-6 (GS) isolate showed reactivity with all isolates tested, but others only reacted with HHV-6 isolates similar to the GS isolate and not with those similar to Z-29 isolate. Restriction enzyme analysis using EcoRI, BamHI, and HindIII revealed that HHV-6 isolates from roseola, bone marrow transplant, leukopenia, and an HIV-1-positive AIDS patient from Zaire (Z-29) were closely related but distinct from GS type HHV-6 isolates. Based on the above findings, we propose that, like herpes simplex virus types 1 and 2, the 15 HHV-6 isolates analyzed can be divided into group A (GS type) and group B (Z-29 type).

 

Source: Ablashi DV, Balachandran N, Josephs SF, Hung CL, Krueger GR, Kramarsky B, Salahuddin SZ, Gallo RC. Genomic polymorphism, growth properties, and immunologic variations in human herpesvirus-6 isolates. Virology. 1991 Oct;184(2):545-52. http://www.ncbi.nlm.nih.gov/pubmed/1653487

 

Intravenous immunoglobulin and myalgic encephalomyelitis

Comment on: Intravenous immunoglobulins. [BMJ. 1991]

 

SIR, In his editorial on intravenous immunoglobulin Dr A D B Webster calls for multicentre trials to assess the possible efficacy of this product in various conditions including mvalgic encephalomyelitis. Two such placebo controlled trials have been completed. Unfortunately, the results are conflicting. American investigators treated their patients with 1 g/kg every month for six months. There were no obvious benefits when the treated patients were compared with controls given placebo. An Australian trial used an even higher dose of 2 g/kg over three months. Here there were significant benefits in both physical and psychological wellbeing in the treatment group.

You can read the rest of this comment here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670935/pdf/bmj00145-0062d.pdf

 

Source: Shepherd C. Intravenous immunoglobulin and myalgic encephalomyelitis. BMJ. 1991 Sep 21;303(6804):716. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670935/

 

Chronic fatigue syndrome: clinical condition associated with immune activation

Abstract:

There is much conflicting immunological and viral data about the causes of chronic fatigue syndrome (CFS); some findings support the notion that CFS may be due to one or more immune disorders that have resulted from exposure to an infectious agent.

In the present study, flow cytometry and several different recognising T, B, and natural killer (NK) cell populations as well as activation and cell adhesion antigens were used to study 147 individuals with CFS.

Compared with healthy controls, a reduced CD8 suppressor cell population and increased activation markers (CD38, HLA-DR) on CD8 cells were found. The differences were significant (p = 0.01) in patient with major symptoms of the disease. These immunological indices were not observed in 80 healthy individuals, in 22 contacts of CFS patients, or in 43 patients with other diseases.

No correlation of these findings in CFS patients with any known human viruses could be detected by serology. The findings suggest that immune activation is associated with many cases of CFS.

 

Source: Landay AL, Jessop C, Lennette ET, Levy JA. Chronic fatigue syndrome: clinical condition associated with . Lancet. 1991 Sep 21;338(8769):707-12. http://www.ncbi.nlm.nih.gov/pubmed/1679864

 

Clinical and pathogenetic observations on children with chronic mononucleosis

Abstract:

Epstein-Barr virus is seldom the causative agent of a prolonged atypical illness, known as chronic mononucleosis syndrome, characterized by a persistent pattern of clinical manifestations and by a defective immune response to specific viral antigens. This paper refers about 6 children for whom clinical and serological findings suggest the chronic Epstein-Barr virus infection. The authors believe that this chronic state might be explained by the unusual antibody pattern to EBV virus, with the persistent presence of anti-EA and the absence of anti-EBNA titers, expression of a reduced EBV-specific cytotoxic T cell activity.

 

Source: Cataldo F, Ammatuna P, Bellia L, Sammartano F, Violante M, Albeggiani A. Clinical and pathogenetic observations on children with chronic mononucleosis. Pediatr Med Chir. 1991 Sep-Oct;13(5):489-94. [Article in Italian] http://www.ncbi.nlm.nih.gov/pubmed/1664943

 

A comparative psychiatric assessment of patients with chronic fatigue syndrome and muscle disease

Abstract:

The psychiatric status of patients with chronic fatigue syndrome (N = 34) and muscle disease (N = 24) attending a general medical clinic was studied. Among fatigue patients 14 (41.2%) were cases and a further 9 (26.5%) were subcases of psychiatric disorder as defined by CATEGO. A variety of diagnoses was found. Significantly fewer of the muscle patients had a psychiatric disorder with 3 (12.5%) being cases and 1 (4%) a subcase. The relative risk of psychiatric disorder in patients with chronic fatigue syndrome compared to patients with muscle disease was 3.3:1.

 

Source: Wood GC, Bentall RP, Göpfert M, Edwards RH. A comparative psychiatric assessment of patients with chronic fatigue syndrome and muscle disease. Psychol Med. 1991 Aug;21(3):619-28. http://www.ncbi.nlm.nih.gov/pubmed/1946850