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Surprisingly good outcomes for people who get ME/CFS after Mononucleosis (Glandular Fever)

Sometimes ME/CFS emerges after mononucleosis, or glandular fever. Simon McGrath shares results from a long-term follow-up study from Haukeland University Hospital in Norway …

results“When will this end?” It’s a question that most ME/CFS patients have probably asked themselves and their doctor many times. I certainly have.

Yet there is astonishingly little hard data on recovery rates from this illness or on how much patients improve, and the evidence there is doesn’t give too much hope.

Step forward a long-term follow-up study that shows unexpectedly good rates of improvement for younger people who developed ME/CFS after infectious mononucleosis (glandular fever) – though the results are hardly spectacular.

Around 11 years on from getting sick, just over half of all ME/CFS patients were able to work part or full-time, though fatigue levels remained high:

Longitudinal follow-up of employment status in patients with chronic fatigue syndrome after mononucleosis

The study was led by Dr  Morten Nyland and comes from the Neurology department of Haukeland University Hospital in Norway, site of the famed Rituximab pilot study. In fact two of the authors of this new paper were part of that pilot study.

And although this wasn’t a trial, patients were encouraged to use self-management (pacing/activity management), and the authors concluded that this probably contributed to the relatively good outcomes.

How the study worked (important)

An ideal study would take a bunch of patients and follow them at consistent time points, say the start of the illness, and then five and 10 years later. In this case, though, researchers made the most of pre-existing data to access a large group of patients who were followed up at very different times in their illness, an approach using two contact points that still yields invaluable results.

“Contact 1” was the first time the patient was seen by the specialist ME/CFS clinic at Haukeland University Hospital, any time between 1996 and 2006.

“Contact 2” was a follow-up questionnaire sent to all patiets in 2009, an average of 6.5 years later. There was huge variation in follow-up time between patients, for example at the second and final contact in 2009 one patient had been ill for 24 years and another only five years. The study had data at both contact points for 92 patients, making this one of the largest follow-up studies going.

At the initial contact, patients had been ill for an average of nearly five years, and again that hides a lot of variation. Half had been ill for 3.2 years or less, a quarter for under two years. The higher average was because some had been ill for a very long time. The patients were also relatively young (the average age was 24 years), reflecting the age profile of infectious mononucleosis, the ‘kissing disease‘, which particularly affects young adults and teens.​

Over half of all patients were employed at final contact

Pleasingly, the study used employment status as the clear-cut, objective primary outcome — and arguably the ability to earn a living is the outcome that matters most to patients. The graph below shows a lot of improvement between first and second contact, with an average gap of six years, though the gap will vary a lot between patients.

Unemployment is in red while employment (full-time or part-time) or being a student is in green. Onset is when they got ill, Contact 1 is typically five years later, and Contact 2 typically another six years on.

Clearly things have improved for many patients, but the overall situation at Contact 2 remains a great deal worse than onset.

Nyland work status at contact 2

Note that half of those employed at Contact 2 were working full-time, compared with only 1 in 10 at Contact 1, so presumably there has been an increase in hours worked per person, as well as more people working.

Caution: It’s possible that 11 years from onset (age 35 vs. age 24 at onset) some people would not be working anyway due to raising families so unemployment might not be zero even for a healthy group. And employment at onset wasn’t split into full-time/part-time.

How patients said their overall health had changed

The study also asked patients how their overall health had changed since Contact 1 (their first visit to the clinic). Most patients said they had improved, 12% reported they had got worse.

Nyland cgi stuff.bmp

Fatigue was also rated at both Contact 1 and Contact 2 using the Fatigue Severity Scale which gives an average score ranging from 1.0 (no fatigue) to 7.0 (maximum fatigue); any score of 5.0 or higher counts as severe fatigue. The average score at Contact 1 was 6.4, falling to 5.0 at Contact 2 — so even after this improvement the group as a whole was right on the threshold of severe fatigue.

Different degrees of improvement

The study measured ‘improvement’ in several different ways. As well as change in employment status, they looked at self-rated improvement (including an option of ‘recovered’) and change in fatigue scores.

You can see that ‘improvement’ ranged from 70% reporting any improvement, to 32% moving into employment, and 13% who rated themselves as recovered.

Nyland, relative improvement

Most people improved, even those who hadn’t improved at Contact 1.

Another encouraging point was that of the 26 people who said they had already improved at Contact 1, 25 improved again by Contact 2. And of the 38 who reported they hadn’t improved before, 25 (66%) improved by Contact 2. 

Fatigue improved much less than employment status

One slightly strange finding, which the authors didn’t comment on, is that average fatigue levels fall rather modestly compared with the percentage improving in employment status. While 32% of patients were able to start working, fatigue scores only fell from 6.4 to 5.0.

It seems likely that this in part is down to people getting back to work but still struggling, so that their level of fatigue doesn’t improve as much as it might.

Interestingly, although 28% were working full-time only 13% rated themselves as ‘recovered’, which supports the view that some people are improving and choosing to work full-time despite not being completely well, and may still be struggling quite a lot.

What ‘predicts’ return to work/improvement over time? (not a lot)

Overall, this important new study shows that outcomes for younger people who develop ME/CFS after mono are not great, but are probably better than expected. Around half were in work 11 years after onset, though fatigue remains high for most.

What might be driving this improvement?  The authors ran some fancy analysis to see what features (such as symptoms and age) predicted being in employment or an improved fatigue score at the final contact. It turned out that only lower joint pain at Contact 1 was associated with later employment, but the effect was small.

Similarly, low joint pain and depression at Contact 1, and better eduction, were predictors of less fatigue at Contact 2 — but again the effect was small.

Surprisingly, length of illness was not an important predictor of employment or fatigue. Generally those with shorter illnesses are seen as having a better chance of recovery, but that doesn’t appear to have been the case here.

It’s possible that outcomes for ME/CFS after mono are better than after other triggers. I’ll give the last word to the authors themselves, who suggest that both pacing/activity management and financial support through sickness benefits were likely to have played an important role to improvements:

“Self-management strategies, long-term sickness absence benefits providing a stable financial support, in addition to occupational interventions aimed at return to work were likely contributors to the generally positive, prolonged outcome.”

 

Simon McGrath tweets on ME/CFS research:

Phoenix Rising thread discussing this paper, including the more detailed post that led to this blog.

Donate to Phoenix Rising – help keep the lights on!

{ 78 comments… add one }

  • MeSci February 7, 2015, 1:12 pm

    Also bear in mind, @Hip, that IIRC 'recovery' was not objectively measured in this study but self-reported. This message cites a small study in which self-reported recovery did not correlate with normal health.

    It's not that people don't want to recover; it's that we want the full facts, warts and all.

  • Hip February 7, 2015, 3:05 pm
    MeSci

    What people object to are the suggestions that our illness can be treated through psychology or exercise.

    Well, yoga is a bit more than just exercise, it is a method of cultivating the mind through the body, yet in this recent thread, there were quite a few strong objections to the plausibility of a news story about one ME/CFS patient who felt they had recovered through yoga and dietary changes.

    As this Google search indicates, yoga can modulate the autonomic nervous system and vagus nerve, so given the autonomic dysfunction in ME/CFS, and given theories like Michael VanElzakker's which postulate that a vagus nerve infection causes ME/CFS, it becomes less surprising perhaps that yoga may, in some subset of patients, have benefits.

    Prior to developing ME/CFS, I did quite a bit of yoga (in the days when yoga didn't have the more "commercial" and somewhat secular packaging it often has now), and I can vouch for the fact that yoga can have profound spiritual and calming effects on the mind. That was the main reason I did it.

    When my ME/CFS was at its worst, though, I was far too weak physically to do more than one or two yoga asanas (yoga poses), so I can certainly appreciate that yoga will be impossible for many ME/CFS patients. However, that does not rule out the possibility that some patients may be able to do some yoga, and that out of those who can, some small subset, or even just a handful of patients, might benefit from yoga.

    Reading that press article about a possible ME/CFS recovery from yoga has made curious about trying it, because due I think to various medications I take, my ME/CFS has improved quite a bit over the last few years, especially in terms of my physical stamina (but my mental stamina is still very poor), so now I would be capable of doing some yoga.

    I should add that for me personally, I am looking at this from a scientific point of view, ie, I want to know the medical truth of the matter, rather than a political point of view.

    The political view is different: it revolves around the dishonest and manipulated GET/CBT studies which purport show some patients can recover for ME/CFS using these therapies, when in fact the authors of these studies have done things like dishonestly redefined the meaning of the word recovered in the "small print" of the study, so that they can falsely claim that exercise therapy leads to recovery.

    Politically, ME/CFS patients tend to be vehemently against the notion that a physical exercise might be beneficial for ME/CFS, and I total concur with this vehemence. In fact I spent a lot of time writing comments (like this one) on the articles about GET/CBT, where I did my best to expose the lies behind the GET/CBT studies. So I do my bit in the political battle against the GET/CBT nonsense.

    However, there is also the maxim that "truth is the first casualty of war," which means that anything which looks remotely like physical exercise may get shot down by ME/CFS patients in the flak of battle.

    I tend to be more interested in the truth rather than political spin. Spin is what the Wessely school depend on, because there is little truth behind GET/CBT.

  • MeSci February 7, 2015, 6:37 pm

    @Hip, I have not dismissed the possibility of yoga bringing benefits, but a cure seems implausible.

    I am, however, completely open to the possibility of a cure through diet, and have blogged on the subject as well as posting info in my profile. Diet is a physical treatment and has huge effects on the gut microbiome.

    Some people are sceptical of this too, but that doesn't mean that they believe ME is incurable.

  • Aidan Walsh February 20, 2015, 6:00 am

    'internal ionisation radiation injuries' broken cromosones/translocations has nothing to do with ebv 'myths' let's get to the truth on what these strains of radiation really are now…activated antibodies are ebv cmv HHv6 etc etc

  • dancingstarheart February 24, 2015, 8:11 am

    I would have been the exception if the study expanded to year 14 for me. Mild relapse at year 8 (misdiagnosed as depression), moderate at year 14 (cut work back to 32 hours) . Had substantial debilitating relapse year 15 1/2 (had to quit work) then in year 20 developed into progressive decline until present, 95% bedbound similar to when I originally got sick at age 15. Year 24, I found follicular b cell non-hodgkins lymphoma in nasolabial area (aka lower tear duct gland) and throat lymph nodes ( many anecdotal reports of cancers in these areas for % of ME patients). Rituximab temporarily got rid of cancer, ME symptoms worsened due to chronic multiple viral infections acquired during Rituximab treatment.

  • Aidan Walsh March 21, 2015, 3:34 pm

    There are no strict criterias in CFS/M.E. diagnosis numerous patients fall between the cracks…They don't even have the illness at all…

  • Mel9 March 28, 2015, 12:49 am
    Woolie

    @Gingergrrl, what I meant was this: what if your prognosis depends not on your age, but on the nature of the event that triggered your onset?

    Now, we know that post-EBV ME is more common in younger than older people. This is because most people – with some exceptions like yourself – have encountered EBV by the time they get to their mid 30s, so ME occurring after this age is only rarely going to involve EBV/mono as the triggering event.

    If post-EBV ME has a better prognosis than other types of onset, then that younger group – which contains more EBV-onset cases – might show better recovery for that reason. Not because they're younger as such, but because more have EBV as their onset.

    I don't know if that's the case at all. But its a possibility. It does seem to me that there are mutliple ME's. Acute onset ones do seem to have a better prognosis than gradual, and I think this is probably because they reflect different disease processes.

    Is positive EBV antibodies common?

  • Woolie March 29, 2015, 11:35 pm
    Mel9

    Is positive EBV antibodies common?

    Yes, I believe so, @Mel9. I read somewhere that more than 95% of the adult population is EBV antibody positive.

  • freshbrew April 23, 2015, 2:28 am

    So, I am sort of kidding here, but maybe not really?…….in the fact that I think my only hope of improvement may be to kiss someone with mononucleosis so I can get it. I am a cfs/m.e. sufferer looking for answers on a slow decline since 1991. Now bedbound much of time. Tried all treatments western and eastern medicine offered. Had hopes to try Rituxa_____( spell) chemotherapy one day but saw some bad result outcomes in some on it. So this article looks like mononuclosis may be the better route. I ve been on all the antivirals and most recently Valcyte 900 mg qd. No improvement. Mononucleosis may make my body kick into proper immune gear? I must say i truly doubt this would be the good outcome but willing to try anything after all these years of living dead with m.e.

  • Esther12 April 23, 2015, 2:32 am
    freshbrew

    So, I am sort of kidding here, but maybe not really?…….in the fact that I think my only hope of improvement may be to kiss someone with mononucleosis so I can get it. I am a cfs/m.e. sufferer looking for answers on a slow decline since 1991. Now bedbound much of time. Tried all treatments western and eastern medicine offered. Had hopes to try Rituxa_____( spell) chemotherapy one day but saw some bad result outcomes in some on it. So this article looks like mononuclosis may be the better route. I ve been on all the antivirals and most recently Valcyte 900 mg qd. No improvement. Mononucleosis may make my body kick into proper immune gear? I must say i truly doubt this would be the good outcome but willing to try anything after all these years of living dead with m.e.

    Not a good idea. There's only evidence that mono increases the risk of ill health. People who caught it are on average worse off than those who did not, even though many of those who catch it recover. I don't think that anyone would consider this as a treatment.

  • Woolie April 23, 2015, 12:05 pm

    @freshbrew, you have probably already come into contact with the virus anyway. Most of us have by age 35 (lots of people get it without symptoms).

  • freshbrew April 26, 2015, 9:45 pm
    Esther12

    Not a good idea. There's only evidence that mono increases the risk of ill health. People who caught it are on average worse off than those who did not, even though many of those who catch it recover. I don't think that anyone would consider this as a treatment.

    Thank you, esther. I agree.
    I guess after looking for answers since 91. now completely disabled at age 47 from m.e./ cfs desperation sinks in.

    You are right in that taking on mono for a cure is not the answer.

    In the same context, i will find it greatly surprising if research outcomes are good for m.e./ cfs long term sufferers taking chemotherapy ( rituxamib- spell?) have a positive outcome.
    I had hope from a woman posting somewhere on this site receiving the chemotherapy treatment from a md at LPCH that she was feeling great ……for bit.

    But from the updates she seemed to deduce that the great feeling was from the prednisone( steroids) accompanying the rituxamib.

    I think i remember euphoria can be a side effect of steroids amongst other things.

    Sad for her. I like hearing when others feel better.

  • freshbrew April 26, 2015, 10:20 pm
    Woolie

    @freshbrew, you have probably already come into contact with the virus anyway. Most of us have by age 35 (lots of people get it without symptoms).

    Thank you, Woolie.
    I did not know this.

    You all educate me so much:)

    I had always tested negative for mono ( blood values) so this is good to know.

    Doesnt surprise me though.

    Not sure i trust some lab values anymore, positive or negative.

    Seems my auto antibodies after long term m.e./ cfids/ hhv6 effect my blood values in a inexplicable way.

    I am curious if you or anyone else has thought they have had a false positive lyme test?

    Especially when the" lyme" igm is positive years from each other but never the igg.

    My igg has never turned positive for lyme.

    And per my extensive research and interviews with specialists including llmds,

    the igg should turn positive after you have lyme disease for more than 2 weeks.

    My positive lyme igm s were never accompanied by excaberated symptoms or exposure to ticks.

    Positive " lyme" igm in 2011 and 2014.

    One was western blot at stanford and one was igenix more sensitive.

    Many thanks for your thoughts & sharing Woolie and all.

  • Woolie April 26, 2015, 11:21 pm
    freshbrew

    But from the updates she seemed to deduce that the great feeling was from the prednisone( steroids) accompanying the rituxamib.

    @freshbrew, I don't know much about the testing, as its not available at all where I live. But I'm currently on steroids (25mg per day), and they work. I don't feel euphoric or anything like that. But they suppress immune activity, so make all the immune-related symptoms go away. Which is most in my case. BUT they only work while you're on them, and there dangerous long term. Also, no-one has any idea whether they will help the underlying disease or make it worse in the long run.

    My choice is to take them now, because I spent two months in bed due to a bad relapse, and was about to lose my job. So figured I didn't have a whole lot to lose.

    If nothing else, the dramatic therapeutic effect of the steroids has helped persuade my doc I have a real illness, which he thinks is autoimmune related.

  • Chrisb September 14, 2015, 12:09 pm

    Since all those interested in the subject are probably aware of this thread, I wonder if I could raise here an issue which has puzzled me for years.

    The title of the study which Simon posted suggests that mononucleosis and glandular fever are entirely synonymous. As far as I can see Pfeiffer's glandular fever was described in 1889 to describe a condition with a particular set of symptoms with which we are familiar. This followed on from the Russian Filatov's earlier description and naming of a similar condition in 1885. In 1920 the term infectious mononucleosis was coined to describe the condition in which abnormal monocytes were observed. Although not all patients fitting the original description of glandular fever were found to have observable abnormal monocytes, and thus could not be shown to have infectious mononucleosis, the terms seem subsequently to have been regarded as entirely interchangeable. This seems to have been extremely sloppy thinking and any sensible naming protocol should have resolved the issue. It would seem that there were" infectious- mononucleosis glandular fever" patients and "non infectious -mononucleosis glandular fever" patients.

    Instead of this the non infectious-mononucleosis glandular fever patients were relegated to having merely "a glandular fever like illness", which seems to be a second class diagnosis. This must be wrong. They still had glandular fever within the terms of the original description. It just wasn't within the description of infectious mononucleosis. There seem to have been attempts by observant researchers and clinicians to use the term "atypical glandular fever", which is accurate, but such usage seems by no means universal and I am not sure whether it has any recognition in naming protocols. It is a strange protocol which allows you to describe a subset of patients, claim the entirety of the name, and eject the remainder of the patients.

    I realise that I have omitted subsequent developments regarding EBV and CMV but I don' believe that this alters the basic proposition.

    I don't know what proportion of cases of glandular fever would be regarded as atypical. Let us assume for the sake of argument that it is 20%. (It may be much less). I get the distinct impression that, in terms only of glandular fever sufferers, the atypical form is overrepresented on this forum. Its only an impression and may be wrong. It would be interesting to know.

    If I am completely wrong, as I may be, I am sure someone will put me right and point me in the right direction.

  • Hip September 14, 2015, 3:57 pm

    @Chrisb
    I don't know anything about this, but I just checked, and apparently in the illness of mononucleosis, there are no abnormal monocytes. In the blood of mononucleosis/glandular fever patients, cells with large, irregular nuclei can be seen, and it was originally unclear whether these were abnormal monocytes or abnormal lymphocytes. But it is now known they are abnormal lymphocytes.

    The name 'atypical mononuclear cell' was given when it was not clear if the abnormal cells were abnormal lymphocytes or abnormnal monocytes. It is now known that they are mainly T lymphocytes which are responding to virus-infected B cells.

    Source: Peripheral blood in infectious mononucleosis (glandular fever)

    Note: peripheral blood mononuclear cell (PBMC) = any blood cell having a round nucleus, as opposed to a lobed nucleus. Examples of PBMCs include: lymphocytes, monocytes and macrophages.

    I am not sure if there is any relationship between the appearance of abnormal lymphocytes in mononucleosis, but here it says:

    Some people with ME/CFS have abnormally shaped white cells (atypical lymphocytes), particularly following glandular fever.

  • Chrisb September 14, 2015, 4:39 pm

    @Hip
    Thanks for that Hip. I should clearly rely on better sources. I suspect that the point I am trying to get to is that Glandular Fever was originally diagnosed on empirical grounds before blood tests were available to distinguish between subtypes. At the point when blood tests became available there needed to be questions about those who fulfilled the criteria of Glandular Fever but not of mononucleosis.

    This all seems potentially very relevant in that it is the B cells which are clearly abnormal in mononucleosis but apparently normal in atypical glandular fever, despite the symptoms being pretty much identical. The consultant physician who diagnosed my atypical glandular fever told me that there was a narrow window in which the tests were positive and if this window was missed tests would come back negative. In those circumstances a diagnosis should be made purely on the symptoms. But that was 35 years ago and things might have changed! On the other hand not all change is for the better.

    It would seem to open the possibility of a different immune response allowing the chronicity of the illness. I shall have to try and refine the ideas before putting them to Jonathan. I am sure he will know. This is why I think it would be interesting to know the prevalence on this forum of those with the "glandular fever like illness" and what the ratio of them is to those diagnosed with EBV

  • Hip September 14, 2015, 4:44 pm
    Chrisb

    The consultant physician who diagnosed my atypical glandular fever told me that there was a narrow window in which the tests were positive and if this window was missed tests would come back negative.

    What is the actual difference between atypical glandular fever / mononucleosis, and normal glandular fever / mononucleosis?

  • Chrisb September 14, 2015, 4:54 pm
    Hip

    What is the actual difference between atypical glandular fever / mononucleosis, and normal glandular fever / mononucleosis?

    The blood tests all come back normal despite the symptoms being identical to mononucleosis. For many years before the availability of google I used to think it was merely a condition that looked like glandular fever but couldn't be proved to be. However there are references in the literature which I shall try and find and post links. Someone in either the north of England or Scotland studied a cluster of cases to which the name was attached.

  • Hip September 14, 2015, 4:58 pm
    Chrisb

    The blood tests all come back normal despite the symptoms being identical to mononucleosis.

    Which blood tests? Do you mean EBV or cytomegalovirus IgM antibodies? Or microscopy tests looking for abnormal blood cells?

  • Chrisb September 14, 2015, 4:59 pm
  • Chrisb September 14, 2015, 5:11 pm
    Hip

    Which blood tests? Do you mean EBV or cytomegalovirus IgM antibodies? Or microscopy tests looking for abnormal blood cells?

    That I cannot answer. In my case I had armfuls of blood taken for testing. I would think every test was done that was available in about 1990. I had an excellent consultant at that time. It was the original consultant physician ten years earlier who told me that about atypical glandular fever.

  • Hip September 14, 2015, 6:31 pm
    Chrisb

    That I cannot answer.

    I don't mean your blood tests, but rather the tests and blood markers that distinguish normal versus atypical mono.

  • Chrisb September 14, 2015, 7:04 pm
    Hip

    I don't mean your blood tests, but rather the tests and blood markers that distinguish normal versus atypical mono.

    I still cannot answer. I was relying on what I was told by someone expert in the field in 1980. I discussed the matter with a specialist who was in communication with, inter alia, Mowbray and Behan, and who was my consultant until 1992, when the NHS closed such clinics. In those days one did not need to do ones own research. The doctors were far better at it.

  • Hip September 14, 2015, 8:27 pm

    OK, well I guess we need to consult Professor Google:

    This paper says the blood parameter that is different in atypical infectious mononucleosis is the percentage of CD8 cells. The CD8 percentage is significantly higher in typical infectious mononucleosis than it is in atypical infectious mononucleosis. All the other parameters tested were the same.

    In particular, the paper says that abnormal lymphocyte percentage is the same in both typical and atypical mononucleosis.

    Apparently atypical cases of mononucleosis can be caused by agents other than EBV:

    Other Causes Of Infectious Mononucleosis

    Acute EBV infection accounts for approximately 90% of infectious mononucleosis. Other causes should be considered when a patient, with suspected glandular fever, has an atypical presentation or risk factors for other causes are present. History, clinical presentation and, when indicated, testing may be required to help differentiate between the causes of infectious mononucleosis.

    Diagnosis & Distinguishing Features:

    Cytomegalovirus
    Pharyngitis, fever, malaise, splenomegaly and lymphadenopathy. May be asymptomatic.

    Acute HIV infection
    Symptoms may be less specific and also include mucocutaneous ulceration, rash, headache or diarrhoea. If risk factors are present, HIV should be considered and laboratory testing arranged.

    Viral hepatitis
    Fever, abdominal pain, jaundice and malaise. Hepatomegaly is common. Pharyngitis, lymphadenopathy and splenomegaly are less likely.

    Toxoplasmosis
    Fever, lymphadenopathy and rash, but rarely pharyngitis. Transmission is usually via cat faeces or undercooked meat.

    Human herpes virus-6
    More common in young children (roseola, sixth disease). Fever of three to five days, widespread rash of macules and papules.

    Source: Laboratory investigation of glandular fever

    So possibly your atypical mononucleosis may have been due to one of these other infectious pathogens.

  • Chrisb September 14, 2015, 9:05 pm
    Hip

    OK, well I guess we need to consult Professor Google:

    This paper says the blood parameter that is different in atypical infectious mononucleosis is the percentage of CD8 cells. The CD8 percentage is significantly higher in typical infectious mononucleosis than it is in atypical infectious mononucleosis. All the other parameters tested were the same.

    In particular, the paper says that abnormal lymphocyte percentage is the same in both typical and atypical mononucleosis.

    Apparently atypical cases of mononucleosis can be caused by agents other than EBV:

    So possibly your atypical mononucleosis may have been due to one of these other infectious pathogens.

    Thank you for that. I would not have thought that there was anything on that list which would have escaped the attention of a major teaching hospital in 1990. It is of course a possibility that the illness was caused by one of these pathogens but that the tests were insufficiently precise to detect them.

    The consultant really did take care. I was admitted to hospital twice , briefly, for tests and had a muscle biopsy done. On one occasion he took me to the lunchtime training talk given by Prof Mowbray and was rather concerned at the discussion of recent potential retrovirus links. I don't think much would have got past him. He introduced me to the expert who considered the muscle biopsy. These were serious people I was dealing with.

    Just to confirm that he thought mine an absolutely core case of ME, I was sent off to Glasgow Southern to participate in one of Prof Behan's trials.

    My impression is that there are still people today receiving diagnoses of glandular fever like illness unconfirmed by blood tests.

  • Hip September 14, 2015, 9:22 pm
    Chrisb

    On one occasion he took me to the lunchtime training talk given by Prof Mowbray and was rather concerned at the discussion of recent potential retrovirus links. I don't think much would have got past him. He introduced me to the expert who considered the muscle biopsy. These were serious people I was dealing with.

    The enthusiasm and dedication of these ME/CFS researchers at that time was amazing. I hope that this level of scientific interest in ME/CFS will reinstate itself in the UK at some point (after we put the disastrous Wessely school, those traitors to science — but good friends to the insurance industry — up against the wall).

    I developed ME/CFS around Mid-2005, and it soon became clear to me that very little good science was going on in the NHS in relation to ME/CFS, just all that Wessely school GET/CBT mumbo-jumbo, so I realized my GP and the NHS in general had nothing to offer.

  • Chrisb September 14, 2015, 9:41 pm
    Hip

    The enthusiasm and dedication of these ME/CFS researchers at that time was amazing. I hope that this level of scientific interest in ME/CFS will reinstate itself in the UK at some point (after we put the disastrous Wessely school, those traitors to science — but good friends to the insurance industry — up against the wall).

    I developed ME/CFS around Mid-2005, and it soon became clear to me that very little good science was going on in the NHS in relation to ME/CFS, just all that Wessely school GET/CBT mumbo-jumbo, so I realized my GP and the NHS in general had nothing to offer.

    I agree entirely. I consider myself fortunate that such people were around when I became ill. When the clinic was closed in 1992ish to make way for some CBT/GET clinic run by therapists supervised by psychiatrists it was made clear that it would be a waste of time to attend.

    It does concern me that Virginia Bottomley was a departmental minister at the time of this act of vandalism.