Posted to Co-Cure Fri, 4 Jan 2002 15:04:45 +0100 by Jan van Roijen

The Sydney ME/CFS Clinical and Scientific Conference
December 2001

Report by Dr. Rosamund Vallings


From 30/11/01 to 3/12/01, I was privileged to attend the Third International Clinical and Scientific Meeting in Sydney, Australia, convened by the Alison Hunter Memorial Foundation to discuss the Medical Practitioners' Challenge in making an informed and accurate diagnosis of Myalgic Encephalopathy/Chronic Fatigue Syndrome. This conference provided a bringing together of enthusiastic cutting-edge researchers and clinicians from around the world. The first day was spent in informal discussion among those presenting papers, and the following 2 days were filled with fascinating and diverse presentations.

The conference was opened by Simon Molesworth, QC, who gave us much food for thought regarding the limited funds available for CFS in Australia, the new clinical guidelines, which are still to be published, but are likely to have a psychological bias, and the need for us all to work together for the common cause of recognition worldwide of this complex illness by education and dedication.

The first session was opened by Anthony Komaroff (Boston, Mass) who gave an overview of the Biology of Chronic Fatigue Syndrome. Of those people presenting with fatigue (such as accompanying depression, anaemia, hypothyroidism etc) about 2% have Chronic Fatigue Syndrome according to the CDC formal case definition. He described an illness of sudden onset of flu like symptoms in up to 90% of these patients. There are marked differences when comparing CFS with depression, as shown by results of neuro-endocrine studies, treatment studies and formal psychological assessment. There is a low prevalence of past history of psychiatric disorder in those with CFS. However, 50% those with CFS do develop psychological illness in the years after onset.

While there is no single laboratory test specific for CFS, there is a growing body of research reporting distinguishing findings, such as low level circulating immune complexes, elevated total complement, increased activated CD8 cells, elevated IgG, atypical lymphocytes, poorly functioning NK cells, low level ANA and abnormalities in the RNaseL pathway.

A number of abnormalities are found in brain and nervous system studies. Using neuro-imaging techniques, MRI has revealed punctate areas of abnormality in 78% cases, particularly in the subcortical areas. SPECTscans have shown defects in perfusion and metabolism. . However these tests are not diagnostic. However there are differences in cognition, not explained by co-existent psychological disorders, in particular there is abnormal cognitive processing and slowed reaction times. There is evidence of autonomic dysfunction, with sympathetic and parasympathetic neuropathy. 50% patients have signs of neurally-mediated hypotension or postural tachycardia syndromes. Most patients have sleep disorder with alpha intrusion into delta wave sleep. There is evidence of neuro-endocrine dysfunction as shown by changes in the HPA axis. Studies have demonstrated reduced CRH production with smaller adrenal glands and a decreased 24 hour urinary cortisol level. Prolactin and growth hormone levels may also be lower.

The effects on the brain are non-destructive and non-progressive, but cause marked dysfunction.

No one infectious agent has been shown to cause CFS. There is however evidence to suggest reactivation of several viral agents such as HHV6. Infectious mononucleosis, Q fever and Lyme disease are likely precursors of CFS. HHV6 affects most humans, with lifelong infection, but the evidence for reactivation in CFS is higher than in controls. This virus can affect neural cells and the CNS, leading to neural sequelae, encephalopathy in immuno-suppressed individuals, and there is good evidence for a strong association between HHV6 and MS.

Treatment of CFS with low-dose tricyclics has been shown to be efficacious in fibromyalgia, and they are widely used in CFS to improve the sleep disorder. Some improvement in health has been reported with CBT and graded exercise.

Professor Komaroff concluded that in view of the above evidence, CFS has an organic basis, and in many of the patients there are abnormalities of the limbic system in the brain and abnormal regulation of the immune system, which is possibly a result of limbic system abnormalities. A single cause seems unlikely, but multiple triggering agents (infections, toxins, stress) could be involved.

Pascale de Becker (Brussels, Belgium) compared the Holmes and Fukuda definitions used in the diagnosis of CFS, in relation to symptomatology, in European patients. The Holmes definition was more strongly associated with symptoms that differentiated CFS patients from those who did not comply with the CFS definitions. 10 extra symptoms were added and this improved the sensitivity, specificity and accuracy for selection of CFS patients. Those fulfilling the Fukuda criteria were less severely affected and this led to some clinical heterogeneity. A new definition therefore would strengthen the ability to select CFS patients, and the incorporation of a severity index would be beneficial for subcategorization.

Don Lewis, a GP (Melbourne, Vic) had devised a questionnaire sent out to patients prior to consultation at his specialised CFS clinic. As well as giving the current clinical picture, and saving the doctor time, this also served as a baseline against which future responses to treatment could be assessed. Analysis of 400 patients revealed the most commonly presenting symptoms in order as being: sleep disturbance, fatigue, cognitive dysfunction, neurological symptoms, mood changes and gastro-intestinal problems. Sex, age and illness duration did not alter this incidence.

Prevalence, demography and natural history of paediatric CFS was discussed by Nigel Speight (Durham,UK). He considered this in his area in North England over a 10 year period. There had been an increase in incidence over the period studied, peaking in 1995. He had studied 49 patients with a range of age from 19 months to 16 years at onset. In 14% there was a first degree relative with CFS and a past history of migraine in 67%. 57% had a first degree relative with a history of migraine. 12% cases were described as mild, 39% as moderate and 49% as severe. Full recovery was seen in 15 cases (31%) of which 2 had been in the severe category, and 7 others (14%) had improved significantly. Average duration of illness in those recovered was 5.1 years. Of those still ill, 7 were still in the severe category (14%). School loss was considerable and was 1.8 years per child on average. He found that there was enormous unpredictable variation in these cases.

Richard Burnet (Adelaide SA) had found that gastro-intestinal symptoms are particularly common in CFS patients, and he noted that they had never been properly assessed. A standard questionnaire with some additional CFS-related questions was given to all CFS-diagnosed patients. Patients were then eliminated from the study if they did not show intolerance to alcohol. 120 patients were suitable for analysis and 56 controls were obtained. 86% CFS and 56% controls had GI symptoms. Abnormalities of oesophagus stomach and bowel were discussed. Bloating and abdominal discomfort after meals was more prominent in CFS patients. Solid and liquid emptying studies were then performed. 91% of the CFS patients had problems of delayed gastric and oesophageal emptying, 89% in the liquid phase and 67% in the solid phase. The main abnormality was delay in the liquid phase, which suggests a central rather than peripheral causation for the gastric delay. Autonomic dysfunction as seen in diabetes tends to cause a delay in the solid phase. The delayed motility may well lead to bacterial overgrowth. The GI problems are unlikely to be due to toxins or mercury poisoning. To treat this condition, care should be taken to separate solids and liquids and nutrition should be looked at carefully. Small frequent solid meals were recommended with fluids given 20 minutes later. Maxolon or cisapride may have a place in treatment.

Bacterial colonosis (BC) was discussed by Henry Butt (Newcastle NSW). He had found that patients have multiple gut symptoms with absence of inflammation apparent in faecal samples. Pain and fatigue tended to be more severe in those with BC than without. He has shown a change in the distribution of gut flora in CFS. The E.Coli count was found to be significantly lower than in healthy subjects, and the lactic acid bacteria Enterococcus spp count was significantly higher. There was also marked decrease in Bifidobacterium in CFS. Changes in GI microbial ecology, particularly low E.coli, are significantly associated with fatigue. There are abundant metabolites from E Coli such as serine, alanine and indole. Tryptophan, a precursor of serotonin comes mainly from these metabolites, as well as some from the diet. Serotonin stimulates peristalsis. With the lowered pH associated with increased lactic acid bacteria, the anaerobes have increased proteolytic activity, and this correlates positively with neurocognitive symptoms. There is also deconjugation of bile acids, so fat emulsification is poor and this leads to fat malabsorption.

Wilhelmina Behan (Glasgow, Scotland) presented an update on current research in CFS, which she described as characterised by myalgia and exercise intolerance with unknown pathogenetic mechanisms. Fatigue has central and peripheral components. Fatigue mechanisms are complex, but in disorders such as MS there is significant decrease in muscle phosphocreatine resynthesis after exercise. Patients suffering from MS, COPD and heart failure were studied as well as those with CFS. The muscle chemistry features associated with fatigue all seem to be the same. There is a general manifestation of problems within the muscles, such as changes in enzymes and muscle mass. She described a pathway for exercise from brain, to nerves, to muscle, to muscle metabolism, and from lungs, to circulation, to muscle metabolism. In CFS there seems to be abnormalities in all these processes. She described two kinds of muscle fibres - 'fast' which are used for bursts of energy, and 'slow' which are used for endurance. In particular she noted that those with CFS had up to 20% less of the slow muscles fibres, which helps to explain why people tire so readily. Deconditioning is not a perpetuating factor in CFS, something else is happening. The muscle involvement includes: weakness, delayed recovery, decreased aerobic activity, mitochondrial abnormalities and metabolic abnormalities. Tests showed that patients are slightly weaker than controls, but they are doing their best. 24 hours after exercise, patients were all worse in strength, and the reduction was most severe after 24 hours. This is because the metabolites are slow at resynthesising. This means that graded exercise is unlikely to be of use. Patients have the metabolites but cannot use them properly, so supplements are unlikely to be of help either.

She discussed the issue of resting energy expenditure (REE). When awake, 30% of energy is devoted to maintaining ion gradients. The REE is elevated in CFS patients unable to exercise, and this may relate to cytokine abnormalities, autonomic dysfunction etc. In relation to cardiovascular involvement, the heart is slow to get going with exercise and remains at a low peak value. This may be due to increased vagal tone or an intrinsic heart muscle effect. Autonomic function may play a role. CNS involvement has been shown in SPECT and MRI scans, and neuroendocrine studies show HPA axis abnormalities. Medical stress can affect the CNS providing a changed micro-environment in the brain and increased permeability of the blood-brain barrier. This can lead to changes in gene expression, which in turn affects production of neurotransmitters. All these events have an impact on the exercise pathway. The whole process is likely to have been precipitated by a severe insult to the body.

Charlie Sargent (Adelaide SA) presented a study showing that increases in plasma lactate concentration with exercise intensity were no different from controls. Results indicated that the production and clearance of lactic acid in CFS patients is normal, and does not contribute to their earlier fatigue and reduced power output shown in this study. Patients have normal physical fitness and there is no physiological basis for recommending graded exercise in the treatment of CFS.

The issue of effects of acute orthostatic stress on cardiovascular and cognitive function in CFS was addressed by Adele McGrath (Adelaide SA). This was a small study on 10 patients and 10 healthy sedentary controls. Blood volume and lean body mass fell within normal limits. It was concluded that postural hypotension did not occur in response to short orthostatic stress in these patients, and acute orthostatic stress did not impair cognitive function.

The diagnosis and treatment of multiple chronic bacterial and viral infections in CFS, FM and GWI were discussed by Garth Nicolson (Huntington Beach,California). These conditions are found to have overlapping symptoms, and a major cause of abnormalities maybe chronic viral or bacterial infections. The infection maybe causative, a co-factor or opportunistic. He is particularly interested in the intracellular bacteria and viruses. Detection is by forensic PCR and gene tracking. He has found that multiple Mycoplasma species are involved in 55% of his CFS/FM patients and the majority have more than one species. These bacteria are also present in other conditions such as GWI and in ALS, there is an 85% incidence. He has also detected reactivated HHV6 in 30% patients with or without Mycoplasma. Some patients were also positive for C.pneumoniae.

Patients with Mycoplasma and/or C.pneumoniae were treated with multiple 6 week cycles of antibiotics (doxycycline, ciprofloxacin, azithromycin or clarithromycin) plus nutritional support. HHV6 patients were treated with immune enhancement. Recovery was slow with 6 cycles being required to provide lasting improvement, at which time those recovered were no longer Mycoplasma positive.

He concludes that subsets of these illnesses have chronic infections, which with appropriate treatment may get a slow recovery. Multiple chemical/biological exposures, including vaccines may be implicated in onset.

Kenny de Meirleir (Brussels, Belgium) gave an overview of the possible immunological pathways that are disrupted in illnesses such as CFS. He presented data suggesting improper activation of 2-5OAS in monocytes in both CFS and chronic MS. (not however in relapsing/remitting MS) This results in inappropriate activation of RNaseL This process ultimately leads to blockade of RNaseL-mediated apoptosis. A complex series of biochemical/immunological events then follows. Resultant RNA fragments are then capable of either activating or down regulating PKR. A subsequent release of NO at high (CFS) rates or low (MS) rates by lymphocytes leads to effects on ion channel, NK cell function, COX2 activation and glutamine release by activated T cells in the brain. The Belgian results suggest that CFS and chronic MS are extremes of an array of dysfunctions in the 2-5A/RNaseL/PKR pathways.

Evidence of active HHV6 infection and its correlation with RNaseL (LMW) protein in CFS patients was presented by Dharam Ablashi (Washington, USA). His team had looked at HHV6 in plasma, CSF and white blood cells. The aim was to correlate HHV6 with presence of the 37KDa protein. The 35 CFS patients studied showed that 65% had active HHV6 infection with varying HHV6 IgM antibody and HHV6 infected PBMCs. In the CSF, 26.7% had HHV6 DNA. Nested PCR showed 34% patients had HHV6 in plasma, but using TaqMan PCR, 48.5% were shown positive in plasma, and 40% in CSF. This test was therefore more sensitive in this assay. HHV6 variant A was identified by TaqMan PCR in almost all positive patients. Variant A tends to be acquired in adult life, variant B in early childhood. Ratio of LMW to HMW(80KDa) protein was detected in 70% PMBC samples. Correlation with HHV6 was significant when the ratio was greater than 4. IgM antibody and PCR correlation was less significant.

Kenny de Meirleir and his group looked at the association between mycoplasmae and the 2-5A/RNaseL pathway in CFS. The hypothesis was that there maybe a co-morbid physiopathological mechanism between Mycoplasma infection and the deregulation of the pathway. 182 mainly female patients, free of antibiotic treatment were enrolled. There was significant correlation. He showed that mycoplasmae are active in stimulating some components of the immune system. They can act as polyclonal T cell and B cell activators. Monocytes produce elastase, which can cleave 80kDa RNaseL thus causing deregulation of the antiviral pathway. It has been suggested that LMW RNaseL may reduce Th1 activity, which implicates susceptibility to infections and a suppressed ability to eliminate intracellular antigens.

Wilhelmina Behan then produced strong contradictory evidence that antiviral gene expression is not increased in CFS. 2 interferon-induced antiviral pathways (2-5A/RNaseL and PKR) have previously been shown to be activated in CFS. However, patients with documented viral illnesses were not included in these earlier studies for comparison. 22 CFS patients, 10 with severe gastroenteritis and 21 controls were studied. The mRNA expressions of 4 genes were evaluated in PBMCs using a standard RT-PCR technique. There was no evidence of any significant difference for any of the genes between those with CFS and healthy controls. Patients with infection however, had activation of both pathways: gene expression for PKR was increased by 9.6 compared to controls and that for the inhibitor RLI was higher by a factor of 17 compared to the 2 other groups.

Minor up-regulation in these pathways may persist for several months after a viral illness. Changes seen in CFS patients may therefore be persisting following an earlier infection. When a group of patients with acute infections is included, the changes in CFS are not significant. Antiviral activation cannot therefore be used to form the basis of a rational test for CFS.

Mohamed Abou-Donia (N Carolina,USA) had looked at stress and combined exposure to low daily doses of pyridostigmine, DEET and permethrin in rats. He found that there was blood brain barrier (BBB) disruption and neurochemical and neuropathological alterations in the brain. The experiment simulated the daily exposure to these chemicals experienced by Gulf War veterans. Control groups were used. Animals subjected to stress alone or chemical treatment alone showed no changes in body weight, brain hexamethonium iodide uptake, brain acetylcholinesterase (AChE) or plasma cholinesterase, but exhibited a slight increase in BBB permeability. There was also a decrease in m2-muscarinic Ach receptor ligand binding. In these groups there was no or minimal neuronal cell death. However animals subjected to both chemicals and stress exhibited dramatic increase in BBB permeability, significant decrease in brain AChE activity, decreased m2-muscarinic Ach receptor ligand binding and significant neuronal death. Histological changes were also present in the liver, and were particularly severe when the combination was used. This work showed significant risk in using low doses of these combined chemicals associated with stress. Leakage through the BBB makes the organism vulnerable to entry by toxins, infection etc.

Objective evidence of brain impairment by chemical exposure was presented by Kaye Kilburn (S California, USA). He described 4 categories of responses relating to brain function: physiological (eg balance, reaction time, vision), psychological (eg problem solving, recall, memory), emotions, feelings, mood states (eg depression, anxiety) and symptoms (eg headache, sleep disturbance etc). 8 physiological and 11 psychological tests were described to assess brain function, and are usefully applied to those who have been chemically exposed. Illustrative examples were discussed, and computerised measuring tools were demonstrated.

A psychiatrist who had had CFS, Nicole Phillips (Armadale, Vic) expressed concern at the way psychiatrists have approached this illness in the past, angering patients, annoying researchers and focussing on using the terms neurasthenia and somatization interchangeably with CFS. She defined these 2 terms, and pointed out how neurasthenia initially was considered a physical illness, but was coined as a psychological condition by the psychiatrists over time, and was then interchanged with somatization disorder when a psychological disorder presents with the patient attributing symptoms to a physical cause. There has been a denial of biological abnormalities, with enormously negative implications for CFS patients. She felt strongly that psychiatrists need to better educate themselves about this complex organic illness.

Ellie Stein (Calgary, Canada) produced useful information to differentiate between CFS and psychiatric disorders such as depression and anxiety. All can present with fatigue and there is often clinical overlap. A co-morbid psychiatric disorder should only be considered if the psychiatric symptoms predated the onset of CFS, if the symptoms are generalised beyond health and quality of life issues affected by CFS or if the symptoms are so severe that they prevent a patient from participating in treatment. When treating anxiety and depression in CFS patients, sensitivity to medication must be remembered. SSRIs, treatment of sleep disorder and CBT may all be useful approaches to consider.

Pathophysiological mechanisms and CFS were discussed by Kenny de Meirleir (Brussels, Belgium). He described this condition as having no single aetiologic agent, but there are a number of predisposing factors leading to abnormalities in the immune system. Viral reactivation and opportunistic infections increase. Resultant ankyrin fragments from pathologically cleaved RNaseL interact with ABC transporters, which become dysfunctional, leading to many of the symptoms of CFS. This is described as an acquired channelopathy. 206 CFS patients were studied and 70% were found to be Mycoplasma positive, and these patients had significantly more cleavage fragments of RNaseL.

He also mentioned the Bijlmer incident, when following this plane crash, 67% were found to be infected with Mycoplasma, and suffered CFS-like symptoms.

Rey Casse (Adelaide SA) used SPECTscans to study regional cerebral blood flow in CFS. He recommended that a triple headed camera be used for accuracy and reliability. 13 CFS patients' scans were compared with 11 people suffering from other conditions with normal scans. Visually, deficit in regional cerebral blood flow was found in the temporal areas in 7 patients, and equivocal in 3. Statistical Parametric Mapping was applied to show location and amplitude of significant focal deficits. Most deficits were found in the brainstem, temporal lobes, frontal lobe and anterior cingulate gyrus.

Autism and CFS were considered by Robyn Cosford (Mona Vale NSW) to be part of the same spectrum of disease, which also included ADHD, in light of her findings of similar neuro-immune and gastro-intestinal dysfunction. Similar trends in urinary amino-acid and organic acid output are typically seen in all these disorders. There are also some similarities in plasma lipid analysis and bacterial faecal studies. She found the children with autism are a more metabolically homogenous group than CFS patients, who typically fall into 5 symptom clusters correlating to metabolic findings. However the subgroup of CFS patients with neuro-cognitive and GI symptoms has similar patterns to autistics, and this could indicate commonality in aetiology. She mentioned the fact that many children with autism have had frequent infections, particularly otitis media prior to diagnosis.

Biochemical anomalies in those with CFS who have visual problems were discussed by Gregg Robinson (Newcastle NSW). It has been found that these patients do have biochemical abnormalities similar to those reported as suffering from a visual sub-type of dyslexia, known as Irlen Syndrome (IS). The same visual symptoms occur in both conditions: headaches, photophobia and concentration difficulties. A large percentage have visual processing problems, and there may be a genetic vulnerability. A number of abnormalities of fatty acid metabolism were described. The bacterial fatty acid C17:0 was found to be positively correlated with eye strain and may indicate the presence of a pathogen, and this anomaly was also found in those with CFS.

Greg Tooley (Burwood, Vic) discussed the possibility that disordered circadian time-keeping may contribute to the development and course of CFS. He described a commonality of symptomatology with jetlag and shift-work related syndromes. 3 studies were presented comparing circadian profiles of sleep activity, core temperature and melatonin secretion in CFS. CFS patients' sleep-activity cycles were significantly phase-delayed compared to controls, which led to sleep disturbance and effects on well-being. Circadian rhythms of sleep-wake, core temperature and melatonin secretion were less effectively synchronised in the CFS group. CFS appears to be associated with both internal and external circadian desynchrony.

Neil McGregor (Newcastle NSW) retrospectively reviewed available data to develop a model of disease processes in CFS. Using factor analysis, 4 symptom groups are recognised in CFS: General CFS, neurocognitive, musculo-skeletal and mood changes. The general symptoms are associated with reactivation of viruses, increased RNaseL fragmentation and infectious symptoms. This group are predominantly cytokine-inducing or pathogen associated events. The other groups represent the host's response or cytokine-mediated symptoms. Reactivation of different viruses is associated with symptom variation, while co-morbid infections increase patient morbidity. Pain is associated with increased metabolite excretion and cytokine mediation leads to release of metabolites from the tissues. As amino acids are lost, fatty acids increase and the patient becomes more reactive.

That food intolerance exists as a co-morbidity in CFS was addressed by Tania Emms (Newcastle NSW). Food intolerances are a non-immune mechanism with no increase in IgE. Food intolerance appears to be a significant factor in up to 30% CFS patients. A chemical to which an individual is intolerant needs to accumulate and reach a threshold before symptoms develop, so reactions maybe delayed over hours or days, and many symptoms may occur. Patients were studied using food elimination and food challenge. 90% reported positive outcome after elimination, with improvement in a number of symptoms. Bowel symptoms in particular decreased. Food intolerance therefore may be of aetiological significance in the development of IBS symptoms in CFS. She concluded that symptom management involving attention to food intolerances is under-utilised but maybe a useful approach.

Ruud Vermeulen (Amsterdam, Netherlands) had treated 150 CFS patients with oral L-carnitine 1gm bid for 6 months. 69% reported improvement in fatigue, pain and cognition. Several other studies followed and using higher doses was not as effective. However all groups showed significant improvement, and plasma free-carnitine levels correlated positively with improvement. Up to 52% patients relapsed at follow up after ceasing treatment. Carnitine is used by all cells in the body, and it was mentioned that particularly high amounts are found in sperm cells. Carnitine is needed for fatty acid and carbohydrate metabolism, and also protects vessel walls against hypoxia.

The use of Acclydine in CFS had been investigated by Pascale de Becker (Brussels, Belgium) Acclydine is a plant sourced alkaloid which has effects on protein structure and metabolism. In particular it leads to the activation of the pituitary to increase release of growth hormone. The GH axis has been shown to be disturbed in CFS, so this alkaloid could be of benefit in CFS. 90 patients were studied and the treatment protocol consisted of 4 weeks Acclydine 250mg qid followed by 4 weeks Acclydine 250mg bid. There was significant improvement in the treatment group with 54% symptom improvement and increased IGF-1. No major adverse events were noted and this could therefore be a safe and useful drug in CFS.

Neville Millen (Deakin, Vic) reviewed the sociological implications of having CFS. The 5 decades of political tensions between ME/CFS sufferers, medical science and State, have created enormous problems and stigma. He argued that the medical profession needs to look beyond set boundaries of its present evidence-based paradigm of care, and adopt a more humane, holistic model of clinical practice for these patients. The government needs to be encouraged to fund research, provide better access to welfare payments and sickness benefits and show more respect for the rights of those with CFS.

Dorothy Morris discussed issues from an educational viewpoint particularly addressing the implications of cognitive dysfunction. She has researched the opportunities afforded those with cognitive dysfunction as part of their CFS in light of their difficulties at tertiary institutions around Australia. The research revealed that no attention had been given to helping those with this condition. There is however some accommodation for fatigue at a tertiary level. It seems that there is a lack of trained personnel in tertiary education who could make assessments and decisions on behalf of those with CFS.

Over the last 10 years in the UK, Nigel Speight (Durham, UK) has been involved in 14 cases of ME/CFS in children in which the families have been subjected to Child Abuse proceedings. He feels this is just the tip of the iceberg, as many other families have been threatened. In 13 of the cases the proceedings were reversed, but one boy was kept in psychiatric care for 7 months. Risk factors were noted where parents were more at risk of being accused of neglect, such as single parenthood, failure of child to respond to 'rehabilitation' and confrontational parents. As a result of these actions many of the children lost faith in professionals or even the parents for failing to protect them, and these children had often developed virtual post-traumatic stress disorder.

A father of a severely ill daughter with CFS presented a poignant account of his family's nightmare experiences. Their daughter was subjected to humiliation and intimidation when she did not respond to 'rehabilitation' alongside patients suffering from anorexia. It was suggested she was not suffering a 'real' illness and she was too sick to speak up for herself. When the parents tried to act on her behalf they were accused of interference. The parents were threatened with action from child welfare agencies, and it was suggested that these caring and well-informed parents were not suitable to be looking after their own daughter. They felt they had been grossly abused by the medical profession.

Simon Molesworth,QC (Hampton,Vic) has found that across the world, many ME/CFS patients report unsatisfactory treatment. Serious social, ethical and legal issues were raised. There is now much credible evidence pointing to biophysical and neurological explanations for CFS, and treatment now needs to be shifted away from psychiatry. Doctors need to accept the reality of the physical nature of the illness, chart the case history carefully and determine suitable treatment options. Monitoring and being alert to the stages of the illness all go toward informed decision making, the sharing of responsibilities and liabilities. Patient and medical practitioner need to form a partnership thus sharing the path to recovery.

Robyn Cosford (Mona Vale NSW) presented 2 case histories. All patients were assessed routinely and in addition had tests for urinary organic acids, faecal analyses and intestinal permeability testing. Each patient showed abnormalities on these parameters. There was evidence for fibrillar and non-fibrillar catabolism, dysfunction of the TCA cycle, abnormal gut bacteria and increased intestinal permeability. Management was based on lifestyle change, counselling, meditation, graded exercise and dietary manipulation. Wheat, dairy foods, additives and foods to which the individual reacted were removed. Supplements were added where appropriate according to test results, and included vitamins and minerals such as B6, magnesium and essential fatty acids. Some 'natural' and prescribed antibiotics were used. There were measurable improvements over 1-5 years.

Richard Schloeffel (Gordon NSW) also presented 2 cases. The first was diagnosed as suffering from CFS and found to be PCR positive for Ch.pneumoniae with positive IgG and IgA antibodies. She was treated with a combination of doxycycline, Nilstat, probiotics, minerals and vitamins for 2 years. She recovered completely and is living a normal life. The second patient had a more complex history with many symptoms, but fitted the CDC definition for CFS. He was suffering diarrhoea up to 40 times daily. He was found to be PCR positive to Mycoplasma fermentens. He was treated similarly, with the addition of tertroxin and thyroxine, as he was hypothyroid after an earlier thyroidectomy. He had persistently low E.coli counts and received 13 donor faecal bacterial infusions per rectum. After 40 years, he is now symptom free with normal bowel function.

The issue of reduced cerebral blood flow was further addressed by Richard Burnet (Adelaide, SA). 16 CFS patients were treated with a combination of Hydralazine 25mg 2-4 times daily (starting at - tablet daily and increasing very slowly), extra salt, 3 litres daily fluid, and supplementation with potassium and magnesium. 10 patients did very well, 3 had no response and 3 stopped treatment because of side effects.

Dan Peterson (USA) discussed immune modulating therapies. He described the immunological model for doing this. Ampligen normalises the abnormal pathways. It is a very safe drug, there appear to be no major side effects and no deaths. It is now in phase 3 in a double-blind trial on 320 patients, and is in fact the only drug for CFS in phase 3. A small phase 3 open label trial is also in progress for 40 very severe patients. He also mentioned several other approaches to treatment which have been tried, including antiviral agents for those who are HHV6 positive. Oral therapy seems ineffective, but IV treatment has proved very helpful. Transfer factor has also shown some benefit in HHV6 patients, and is available at pharmacies in the US. Modafinil, a stimulant has shown marked improvement in fatigue in MS and fibromyalgia.

Group therapy was suggested by Rosamund Vallings (Auckland NZ) as a cost and time effective approach as part of the management of CFS. Some of the difficulties experienced in running such sessions was discussed, and suitable programmes suggested. In NZ these sessions are fully government funded for CFS as long as they have an educational component. Patients have been enthusiastic about this approach and have thus gained coping skills and insight into their illness.

Kenny de Meirleir (Brussels,Belgium) summarised his management approach. He aims to restore immune competence, eliminate or decrease the load of micro-organisms and restore hormonal balance. He is using ampligen on 160 patients, uses antibiotics and occasionally Isoprinosine.

10 posters were presented some covering the research presented orally in more detail.

Wilhelmina Behan (Glasgow, Scotland) showed preliminary evidence that there is cardiovascular impairment during dynamic exercise in CFS, as judged by the cardiac output response to moderate exercise.

Pascale de Becker (Brussels, Belgium) had a poster outlining her department's experience of the aetiology of CFS. Upper respiratory infections do seem to be the most common infections preceding illness in her study. A number of different stressors and consequent immunological and neuro-endocrinological changes can contribute to the onset of CFS.

Pascale de Becker had a further poster providing evidence for a channelopathy in a subset of CFS patients, probably induced by the deregulated RNaseL antiviral pathway.

She had another poster showing the prevalence of Mycoplasma in Belgian CFS patients. This organism was found in 68.7% of a group of 272 patients. M.hominis was the most frequently observed followed by M.pneumoniae, and 17.3% had multiple infections.

Supplementation with serine was shown to have potential for symptom management in CFS by Tania Emms (Newcastle NSW). She indicated that a double-blind placebo controlled trial was warranted after there was significant reduction in symptom expression in 28 patients after 3 months, using 1.3gm L-serine daily.

Ann Harvey (Wellington NZ) had done a meta-analysis looking at cortisol levels in CFS patients. She found that patients seen in tertiary care show more endocrine abnormalities and clinical methodologies seem important in assessment procedures.

A suspected new chronic roundworm parasite was described by Lawrence Klapow (California,USA). He estimated that in sputum of 63% of the 30 CFS patients studied the worm (cryptostrongylus pulmoni) was identified.

C.H.Little (Mt Waverley, Vic) has identified a separate class of immune products (T cell antigen binding molecules) which maybe the basis for the adverse reactions to foods experienced by some CFS patients.

A poster presentation by P Clifton Bligh et al (NSW) concluded that the fall in urinary succinic acid seen in CFS patients was associated with deregulation of energy availability and protein synthesis suggestive of a cytokine mediated nitric oxide mediated change in chemistry. These changes relate to the expression of fatigue.

W.Tarello (Perugia,Italy), a veterinary surgeon, presented evidence of CFS in a horse from the USA, examined in Dubai. The horse was treated with IV potassium arsenite and made a good recovery.

The conference was finally summed up by Peter del Fante (Adelaide SA). He confirmed that CFS is a legitimate illness although the diagnostic criteria do need refreshing. In particular we must recognise that these patients are not 'deconditioned'. He presented the GP perspective in saying that one needs to make a positive diagnosis, provide good patient education and supportive therapy should be offered. The doctor should retain ethical boundaries, be a patient-advocate and work with the researchers. Keeping national patient registers and making CFS a notifiable disease are issues to be considered in the future.

Richard Burnet's final words echoed the consensus of the conference that the brain, limbic systems and gut are implicated in CFS with the causation being usually infection plus a predisposition and various trigger factors.

Tim Roberts (Newcastle NSW) stressed the importance of our being ever watchful for new organisms such as strains of Borrelia and Ehlichia not seen before in Australia, which may be implicated in CFS. He thanked Christine Hunter and Ellie Stein for their tremendous energy and enthusiasm which had made this conference possible.

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