2 Paper: 2006 Lyme Disease Guidelines

Okay. So, let's take a look at these guidelines that so many Lyme disease patients have been talking about.

The 2006 Lyme Disease Guidelines (IDSA) can be found here (full text): http://cid.oxfordjournals.org/content/43/9/1089.full

I'm going to be asking questions and making comments on different sections. Be prepared for some jumping around...

"Late Lyme Disease

Lyme arthritis. Lyme arthritis can usually be treated successfully with antimicrobial agents administered orally. Doxycycline (100 mg twice per day) (B-I), amoxicillin (500 mg 3 times per day) (B-I), or cefuroxime axetil (500 mg twice per day) (B-III) for 28 days is recommended for adult patients without clinical evidence of neurologic disease. For children, amoxicillin (50 mg/kg per day in 3 divided doses [maximum of 500 mg per dose]) (B-I), cefuroxime axetil (30 mg/kg per day in 2 divided doses [maximum of 500 mg per dose]) (B-III), or, if the patient is ⩾8 years of age, doxycycline (4 mg/kg per day in 2 divided doses [maximum of 100 mg per dose]) (B-I) is recommended. 

"It is important to recognize that a small number of patients treated with oral agents have subsequently manifested overt neuroborreliosis, which may require intravenous therapy..."

Oral antibiotics are easier to administer than intravenous antibiotics, are associated with fewer serious complications, and are considerably less expensive. However, it is important to recognize that a small number of patients treated with oral agents have subsequently manifested overt neuroborreliosis, which may require intravenous therapy with a β-lactam antibiotic (see the paragraph below) for successful resolution. Further controlled trials are needed to compare the safety and efficacy of oral versus intravenous therapy for Lyme arthritis."

Given what I wrote in a previous post on the 2000 Lyme disease treatment guidelines, this is a continuation of my questioning this line of reasoning:

How do they determine that someone has neuroborreliosis?

What if it's subtle and not overt?

In the 2000 guidelines, they were urging doctors to look for subtle neurologic symptoms.

To continue...

 "Neurologic evaluation that may include lumbar puncture should be performed for patients in whom there is a clinical suspicion of neurologic involvement. Adult patients with arthritis and objective evidence of neurologic disease should receive parenteral therapy with ceftriaxone (A-II) for 2–4 weeks. Cefotaxime or penicillin G administered parenterally is an acceptable alternative (B-II). For children, intravenous ceftriaxone or intravenous cefotaxime is recommended (B-III); penicillin G administered intravenously is an alternative (B-III). See the recommendations above for treatment of patients with Lyme meningitis for suggested doses of each of these antimicrobials."

Okay well, this is what they have to say about treating Lyme meningitis:

"Lyme meningitis and other manifestations of early neurologic Lyme disease. The use of ceftriaxone (2 g once per day intravenously for 14 days; range, 10–28 days) in early Lyme disease is recommended for adult patients with acute neurologic disease manifested by meningitis or radiculopathy (B-I). Parenteral therapy with cefotaxime (2 g intravenously every 8 h) or penicillin G (18–24 million U per day for patients with normal renal function, divided into doses given every 4 h), may be a satisfactory alternative (B-I). For patients who are intolerant of β-lactam antibiotics, increasing evidence indicates that doxycycline (200–400 mg per day in 2 divided doses orally for 10–28) days may be adequate (B-I). Doxycycline is well absorbed orally; thus, intravenous administration should only rarely be needed."

How are these recommendations for treating Lyme meningitis any different from what was posted in 2000? It isn't - it's the same.

This is also how late stage Lyme meningitis was recommended to be treated in 2000.

In terms of it manifesting as neurologic Lyme disease, the above recommended treatments are for early and not late stage neurologic Lyme disease. The suggested treatment here for both early and late stage neurologic Lyme disease is the same.

Looking back at the research compiled and cited in the 2000 guidelines, how many successful outcomes, i.e. total symptom resolution, were there after using this recommended treatment for late stage Lyme disease?

Where are the follow up studies which show refinement and an improvement in those patients who were treated and failed treatment - not as chronic Lyme patients, which has become a muddy, nonspecific term anyway - but in late stage Lyme disease patients?

Because that's what we are talking about here.

Moving on...

"There was agreement that lumbar puncture is indicated for those in whom there is strong clinical suspicion of CNS involvement (e.g., severe or prolonged headache or nuchal rigidity). Patients with normal CSF examination findings and those for whom CSF examination is deemed unnecessary because of lack of clinical signs of meningitis may be treated with a 14-day course (range, 14–21 days) of the same antibiotics used for patients with erythema migrans (see above) (B-III). Those with both clinical and laboratory evidence of CNS involvement should be treated with regimens effective for Lyme meningitis, as described above (B-III)."

Maybe I'm not reading this right, but what about the treatment for radiculopathy without meningitis?

In the section above that, they are recommending IV treatment for adult patients with radiculopathy OR meningitis,  but here they are saying to give people with suspected CNS involvement the same treatment as those with only an EM rash?

Do you have any idea how many patients I've talked to or read about who had symptoms as those mentioned here who did not get a LP?

From this description, it's saying even if CSF is normal (a high likelihood given how the test only catches 10-30% of all neurological cases of Lyme) and there is a lack of meningitis, patients should be given up to 21 days of oral antibiotics (refer to the original guidelines for this - it's not on this page).

So what happens if a late stage Lyme disease patient has negative CSF and no signs of meningitis but has radiculopathy or even no radiculopathy? I'm guessing they get 14 days of oral antibiotics - 21 days, max. And if they have neuroborreliosis with subtle neurological signs and no positive CSF test, then they would be getting undertreated, I would think.

Okay, onwards...

"Late neurologic Lyme disease. Adult patients with late neurologic disease affecting the central or peripheral nervous system should be treated with intravenous ceftriaxone for 2 to 4 weeks (B-II). Cefotaxime or penicillin G administered intravenously is an alternative (B-II). Response to treatment is usually slow and may be incomplete. Re-treatment is not recommended unless relapse is shown by reliable objective measures. Ceftriaxone is also recommended for children with late neurologic Lyme disease (B-II). Cefotaxime or penicillin G administered intravenously is an alternative (B-III). See the recommendations above on the treatment of Lyme meningitis for suggested doses of each of these antimicrobials." 

Yes, this is the same recommendation that was given in 2000.

Referring to my previous post on guidelines, what do they consider to be "reliable objective measures"?

And then we come to the section we've all been waiting for or wanting to ignore - depending on who is reading along - the Post-Lyme Disease Syndrome section:

" Post–Lyme Disease Syndromes

There is no well-accepted definition of post–Lyme disease syndrome. This has contributed to confusion and controversy and to a lack of firm data on its incidence, prevalence, and pathogenesis. In an attempt to provide a framework for future research on this subject and to reduce diagnostic ambiguity in study populations, a definition for post–Lyme disease syndrome is proposed in these guidelines. 

"There is no convincing biologic evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment regiments for Lyme disease?"

Whatever definition is eventually adopted, having once had objective evidence of B. burgdorferi infection must be a condition sine qua non. Furthermore, when laboratory testing is done to support the original diagnosis of Lyme disease, it is essential that it be performed by well-qualified and reputable laboratories that use recommended and appropriately validated testing methods and interpretive criteria. Unvalidated test methods (such as urine antigen tests or blood microscopy for Borrelia species) should not be used. 

There is no convincing biologic evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment regimens for Lyme disease. Antibiotic therapy has not proven to be useful and is not recommended for patients with chronic (⩾6 months) subjective symptoms after recommended treatment regimens for Lyme disease (E-I)."

So excuse my ignorance, but why have a section on post-Lyme disease syndrome if you cannot even determine what a well-accepted and consistent definition of it is?

And there is already a problem here: If testing is not reliable for B. burgdorferi infections, especially in their early stage - and in particular, if CSF tests are only somewhat reliable in neurroborreliosis in the first two weeks of infection - how can one be certain years later that someone with symptoms has late stage Lyme disease or chronic Lyme disease?

"There is no convincing biologic evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment regiments for Lyme disease?"

No? None? That's a pretty strong statement. Especially given that there are case studies of people with symptomatic chronic B. burgdorferi.

Even from these panelists, I would expect to see reference to "minimal" or "limited" biologic evidence - and mention of a small number of case studies of patients with persistent infections after antibiotic treatment.

Because they are out there. They exist. How can they ignore them?

Here are just a few:

Liegner KB, Duray P, Agricola M, Rosenkilde C, Yannuzzi L, Ziska M, Tilton R,
Hulinska D, Hubbard J, Fallon B. Lyme Disease and the Clinical Spectrum of
Antibiotic-Responsive Chronic Meningoencephalomyelitides. J Spirochetal and
Tick-borne Dis 1997;4:61-73.

Lawrence C, Lipton RB, Lowy FD, Coyle PK. Seronegative Chronic Relapsing
Neuroborreliosis. Eur Neurol 1995;35:113-117.

Liegner KB, Shapiro JR, Ramsay D, Halperin AJ, Hogrefe W, Kong L. Recurrent
erythema migrans despite extended antibiotic treatment with minocycline in a
patient with persisting Borrelia burgdorferi infection. J Amer Acad Derm
1993;28:312-4.

Liegner KB, Rosenkilde CE, Campbell GL, Quan TJ, Dennis DT. Culture-confirmed
Treatment Failure of Cefotaxime and Minocycline in a Case of Lyme
Meningoencephalomyelitis in the United States. Program and Abstracts. V
International Conference on Lyme Borreliosis. Abstr. 63 P. A11, Arlington, VA.
May/June 1992.

Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A, Prokop J.
Survival of Borrelia burgdorferi in Antibiotically Treated Patients with Lyme
borreliosis. Infection 1989;17:355-359.

And that's just a few.

If you're not satisfied with this quantity, more human and animal studies can be found here:

http://lymeinfo.net/medical/LDPersist.pdf

On to evidence to support treatment recommendations...

Differing criteria were used to define treatment failure in the various studies. Most defined “failure” as the persistence of objective clinical manifestations despite therapy, whereas others used the persistence of subjective symptoms.

"There have been at least 9 randomized, prospective trials addressing the treatment of early Lyme disease in the United States [41–43, 137–142]. All studies used erythema migrans as the disease-defining criterion. Eight studies recruited patients with either localized or disseminated early Lyme disease [41–43,137–139, 141, 142], whereas 1 study required disseminated early disease for enrollment [140]. Differing criteria were used to define treatment failure in the various studies. Most defined “failure” as the persistence of objective clinical manifestations despite therapy, whereas others used the persistence of subjective symptoms."

That's interesting. Why use different criteria to define treatment failure in different studies?

"The etiology of residual patient complaints after treatment may include an inflammatory response unrelated to active infection or may be due to alternative disease processes. The possibility that these symptoms may have been related to a tick-transmitted coinfection was not evaluated in any of the studies. Importantly, failure rates were not considered in the context of the high frequency of background complaints present in an otherwise “healthy” population. Both of these factors have likely contributed to a misconception by some that recommended treatment courses are associated with a relatively poor outcome. This has helped to foster highly speculative theories on how B. burgdorferi might survive in patients treated with a standard course of antimicrobial therapy. These issues are discussed in greater detail below in the section on post–Lyme disease syndromes."

This is important information.

A sizeable percentage of ticks are now found to be co-infected with other tickborne diseases. If a patient is bitten by a tick with more than one infection, that can and very likely would affect treatment outcome and persisting symptoms. If you treat one infection - only to neglect treating another, different infection - that patient still needs treatment and is sick.

This is something that requires further research and should not be ignored in developing a comprehensive treatment plan for patients.

"Both of these factors have likely contributed to a misconception by some that recommended treatment courses are associated with a relatively poor outcome."

Actually, no. You don't have look at those two factors.

Anyone reading the 2000 and 2006 treatment guidelines' study summaries for late stage Lyme disease treatment would get the perception that recommended treatment courses are associated with a relatively poor outcome.

Let's go look at two examples from this page again:

"Patients with late Lyme disease associated with prominent neurological features also respond to antibiotic therapy. In trials conducted from 1987 through 1989, 27 adult patients with Lyme encephalopathy, polyneuropathy, or both were treated with iv ceftriaxone (2 g/d for 2 weeks) [93]. In addition to clinical signs and symptoms, outcome measures included CSF analyses and neuropsychological tests of memory. Response to therapy was usually gradual and did not begin until several months after treatment. When response was measured 6 months after treatment, 17 patients (63%) had uncomplicated improvement, 6 (22%) had improvement but then relapsed, and 4 (15%) had no change in their condition."

So right there, the study outcome was that 6 of 27 patients improved but relapsed, and 4 just didn't get any better.  In this study, 37% of the patients did not have "uncomplicated improvement". (What does that mean, "uncomplicated improvement"? Why not use the words "were cured"? )
No, in this study, 37% did not improve at all as far as we know. Some followup report here would be good.

And...

"In an open-label, randomized, multicenter study, 143 evaluable patients with manifestations of late Lyme disease, primarily Lyme arthritis, were treated with iv ceftriaxone (2 g/d for either 2 or 4 weeks) [85]. In 76% of those treated for 2 weeks and 70% of those treated for 4 weeks, symptoms resolved after treatment (the P value was not significant). The most common persistent symptoms were arthralgia, pain, weakness, malaise, and fatigue."

Okay, so 76% of patients treated for 2 weeks and 70% of those treated for 4 weeks, symptoms resolved. Now what about the other 24% and 30% respectively? Their symptoms must not have resolved?

Is having one in three - or one in four patients continuing to have symptoms - a good outcome?

Without even mentioning coinfections or anything else, wouldn't you think that having a quarter to a third of your late stage patients failing treatment is an indication that these recommended treatment courses are associated with a relatively poor outcome?

Is having one in three - or one in four patients continuing to have symptoms - a good outcome?

Okay, on to some early treatment studies:

"Duration of antibiotic therapy for erythema migrans was addressed in a prospective, randomized, double-blind, placebo-controlled clinical trial of 180 patients [142]. Patients were randomized into 3 treatment groups: doxycycline (100 mg twice per day by mouth for 10 days); a single 2-g intravenous dose of ceftriaxone, followed by doxycycline (100 mg twice per day by mouth for 10 days); and doxycycline (100 mg twice per day by mouth for 20 days). The rate of complete resolution of signs and symptoms was similar for all 3 treatment groups in both on-study and intention-to-treat analyses. Despite the potential for B. burgdorferi to disseminate to the CNS in some patients with erythema migrans [145], the addition of a single dose of ceftriaxone to a 10-day course of doxycycline did not improve outcome. The single ceftriaxone dose, however, was associated with a 4-fold increase in the frequency of diarrhea (P < .001)."

Well, shit. That doesn't sound good. But then how does one determine when to give someone treatment for neuroborreliosis when the most effective time to treat it is before it gets into the CNS and brain?

Knowing what I know now, I would rather deal with diarrhea than a CNS infection. Dose me with probiotics and saccharomyces boulardii if you have to, but seriously, if someone had given me the ceftriaxone when I first had the Headache From Hell, maybe I wouldn't be writing this damn blog. I'd be in Paris by now.

"Less than 10% of individuals do not respond to antibiotic therapy, as evidenced by the presence of objective clinical manifestations, and rarely is re-treatment required. In general, patients who are more systemically ill (e.g., febrile with significant constitutional complaints) at the time of diagnosis take longer to have a complete response to therapy."

Wait. Why is this saying that re-treatment is rarely required here, with objective clinical  manifestations - when earlier upstream it says this for late neurologic Lyme disease?:

"Response to treatment is usually slow and may be incomplete. Re-treatment is not recommended unless relapse is shown by reliable objective measures."


What is the difference between these "reliable objective measures" and the presence of "objective clinical manifestations"?

Why aren't patients in this 10% considered treatment failures who have relapsed?

What does it mean that less than 10% of individuals do not respond to antibiotic therapy?

Could it be that the strain of Bb they have does not respond to a specific antibiotic treatment and is resistant?

Could it be these patients' immune systems are unable to clear the infection on its own after stopping treatment?

There is no explanation given here for why these patients are not responding to antibiotic therapy - and here we are, talking about early treatment.

That's right: early infection. Not late stage Lyme disease. Not Post-Lyme. Not chronic Lyme. EARLY.

Also, why not recommend testing for coinfections right here at this point in the recommendations?

"Inadequately recognized CNS infection at the time of institution of antibiotic therapy may be the explanation for antibiotic failures in some circumstances."

Well see, now we're talking. This has been my concern for some time. Any suggestions as to how to address this problem?

Next up... Background and Diagnosis of Late Neurologic Lyme Disease:

"Late neurologic Lyme disease may present as encephalomyelitis, peripheral neuropathy, or encephalopathy [149–152, 208–212]. Because most patients with Lyme disease are now diagnosed and treated early in the course of infection, these more indolent forms of neurologic Lyme disease are quite rare."

Is this an accurate statement?

Dr. Brian Fallon has said one way in which Lyme disease patients are falling through the cracks in the system is because the US does not have regular and adequate testing for neuroborreliosis.

The Institute of Medicine's recent summary report on Lyme disease included this mention on testing for neuroborreliosis in the US:

"One scientific gap is the testing of cerebrospinal fluid for antibodies. Europeans measure intrathecal production of antibodies by measuring antibodies in CSF and comparing these results against the concentration of antibodies in the serum to produce a ratio. U.S. Scientists have not had a sufficiently large population in which to evaluate the efficacy of this approach because fewer cases of neuroborreliosis are documented in the United States as compared to Europe and CSF sampling is not routinely done in patients with Lyme disease. The absence of this type of testing is a gap in diagnostics for neuroborreliosis caused by B. burgdorferi in the United States."


The US has not particularly specifically been looking for neuroborreliosis when and if it's been looking at Lyme disease in a patient. The implication here is that the US is not documenting neuroborreliosis cases and testing for it is not routine. 


The argument is circular: The US doesn't have that many cases of neuroborreliosis because the US hasn't found that many cases of them, but then again, it may not have found that many cases of neuroborreliosis because it's not routinely tested for.


And for those who state that in Europe it is more routinely tested for because their strains produce early neuroborreliosis and the American strain of Bb doesn't, you must have missed the early summary posts from the IOM:


"Although the differences between presentations of European and American Lyme neuroborreliosis have been stressed over the years, they may have been overemphasised in the case of early neuroborreliosis (Halperin, 2008). This is also supported by clinical experience in the UK, where between 10 and 20% of patients with serologically confirmed Lyme borreliosis acquired infections abroad, in mainland Europe or USA (HPA, 2011). Clinicians in the UK have noted marked similarities in acute neurological presentations of patients with USA-acquired infection and those acquired in the UK and other parts of Europe (Dillon, O'Connell and Wright (2010)."

How can our measurement of US neuroborreliosis be accurate when it's not being routinely tested for and subtle symptoms may be missed or misdiagnosed as viral meningitis?

How can our measurement of it be accurate when it's not clear how many people in the population at large have contracted Lyme disease in the US?

We have an annual report of 40,000 cases a year in the US that is growing, but those are only reported cases. The actual number is supposed to be higher.

The reported cases are more likely to be those that are caught early and present with a clear EM rash to meet CDC surveillance requirements.

What about people who are misdiagnosed early because people cannot recall a tick bite and are diagnosed with another condition? Like MS? Many researchers write in their own papers that this difficulty with early, accurate diagnosis is an issue, from microbiology students through seasoned professionals through patent holders.

More quotes from the IOM paper:

"Central nervous system manifestations of late neuroborreliosis include encephalitis or encephalomyelitis with tetraspastic syndrome, spastic-ataxic gait disorder and disturbed micturition, which may lead to misdiagnosis with other conditions such as multiple sclerosis if the possibility of neuroborreliosis is overlooked. Clinical awareness of this possibility is crucial, as antibiotic treatment will arrest progression. The degree of clinical recovery following microbiological cure depends on the severity of tissue damage. Recovery may be slow, especially in older patients, and can be incomplete, particularly in those who had been severely affected prior to treatment."

and

"Turning to the literature pertaining to patients with chronic persistent symptoms, Fallon noted a number of areas need additional research. A European study compared patients with neurologic Lyme disease to those with erythema migrans 3 years later and found that 50 percent of those with neuroborreliosis experienced persistent symptoms versus 16 percent of the EM patients (Vrethem et al., 2002).These results suggest that follow up studies on chronic symptoms, rather than focusing solely on early EM, should focus on the subpopulation of patients who present with neurologic or other disseminated symptoms."


Okay. Do I need to say anything more about the relevance of neuroborreliosis and the relationship between not diagnosing and treating early Lyme disease adequately and later more serious chronic and persisting symptoms?


I think not.


Moving on, back to the 2006 Lyme disease treatment guidelines...

"Two-tier (ELISA and IgG immunoblot) seropositivity with serum samples and evidence of intrathecal antibody production to B. burgdorferi are expected [149, 162, 213]. Intrathecal antibody production, however, may persist for years following successful treatment, so this parameter does not provide a useful marker of disease activity [214]. CSF examination typically shows a lymphocytic pleocytosis, a moderately elevated protein level, and a normal glucose level [149, 213]. Sensitivity of PCR for detection of B. burgdorferi DNA in the CSF of such patients is extremely low. MRI of the affected part of the neuraxis can demonstrate areas of inflammation, typically with increased signal on T2 and FLAIR imaging and enhancement following contrast administration [149, 215]."

How many primary care physicians do you know of that are aware of this and test patients with neurological symptoms in this way?

I know that CSF testing is pretty much pointless past the first two weeks of infection, and even during those weeks, it has a low return.

So this has to be a clinical diagnosis leading to heavy treatment early on if you are going to treat it effectively.

"Late neurologic Lyme disease–associated peripheral neuropathy typically presents as a mild, diffuse, “stocking glove” process. Only 9 such patients have been diagnosed by panel members (G.P.W., J.J.H., R.B.N., R.J.D., A.C.S., E.D.S., M.S.K., P.J.K., J.S.B., and L.B.) over the past 5 years. Patients typically complain of intermittent limb paresthesias, and some patients complain of radicular pain. The most frequent abnormality found on neurologic examination is reduced vibratory sensation of the distal lower extremities. Electrophysiologic studies show findings consistent with a mild confluent mononeuritis multiplex [219]. Nerve biopsy reveals small perivascular collections of lymphocytes, without spirochetes [220, 221]. Serum IgG antibody to B. burgdorferi detected by the 2-tier approach is expected in patients with Lyme disease–associated peripheral neuropathy. The absence of antibody should lead to an alternative diagnosis [149]. Because the pathophysiologic process usually occurs outside the subarachnoid space, CSF findings are often normal, without evidence of intrathecal antibody production to B. burgdorferi."

A sample size of 10 doctors when there are over 8,000 members of the IDSA is, well, suffering from the small numbers problem.

Why is it relevant to know panel members have diagnosed only 9 such patients with peripheral neuropathy? This says something about their rate of diagnosis, but nothing about the rate at which this condition is found among all patients diagnosed with Lyme disease and suspected to occur and how many cases thousands of doctors may encounter each year.

A sample size of 10 doctors when there are over 8,000 members of the IDSA is, well, suffering from the small numbers problem. We need to see a bigger sample size than that to get a better idea of disease distribution and sequelae.

And even then, remember what is stated above this quoted paragraph? Neuroborreliosis is not routinely diagnosed and tested for in the US.

Below this section, they begin describing all the same studies in treating late stage Lyme disease patients that were mentioned in a previous post on the 2000 Lyme disease treatment guidelines.

The same studies with small study groups. The same studies with a large number of treatment failures and patients with relapses, persistent symptoms, and incomplete resolution of their symptoms.

Six years later. 2006. No new studies. No new information. No improvement in the percentage of patients with lingering symptoms after treatment, relapses, or incomplete recoveries.

No reported follow up on those groups which I could see.

Please point them out to me if you see any follow ups. I'm concerned about those patients and hope they are okay - at least hope they are doing better.

"It was concluded that Lyme encephalopathy may be associated with active infection of the nervous system and that the infection can be treated successfully in most patients with a 30-day course of intravenous ceftriaxone. Whether a 30-day course is superior to 14 days of treatment is unclear. Although the data are much more limited, children with neurocognitive abnormalities attributed to Lyme disease also appear to improve after 2–4 weeks of intravenous ceftriaxone [239]."

I say 30 days is a small price to pay compared to years of misery. If you can get diagnosed and treated early on after the bite, 30 days is manageable.

Sure as hell beats the months of IV treatment some LLMDs give patients.

Seriously, you get Lyme disease and know early on it's in your CNS and brain? Do the antibiotics.

I mean, what's the option? Letting bacteria screw into your brain? I don't think you want to take that option.

"Bartonella DNA has been found in some Ixodes species, but there is no convincing evidence that Bartonella infections can be transmitted to humans by a tick bite [260]."

People are getting Bartonella somehow. If it shows up on their tests as positive, treat them for Bartonella.

For all we know, a flea from their cat bit them and gave it to them. It may have come from a tick bite, too. Either way, treat the patient.

Here we come to the part that pisses off a great number of Lyme disease patients...

Ready?

"In many patients, posttreatment symptoms appear to be more related to the aches and pains of daily living rather than to either Lyme disease or a tickborne coinfection. Put simply, there is a relatively high frequency of the same kinds of symptoms in “healthy” people. For example, 20%–30% of adults complain of chronic fatigue [261–263], and in the 2003 National Health Interview Survey, the frequency of doctor-diagnosed arthritis cases among adults was 21.5% [264]. A study in England found a point prevalence of 11.2% for the presence of self-reported chronic widespread pain among adults that was frequently associated with feelings of depression and anxiety, fatigue, and somatic symptoms [265]. A recent study of the general adult United States population estimated a point prevalence of self-reported serious pain (level 3) to be 3.75%–12.10%, depending on the assessment tool used; for level 3 emotional or cognitive dysfunction, it was 2.17%–3.42% [266]."

If 20-30% of all adults had what Lyme disease patients have been diagnosed with - CFS - they would not be able to work.

Are we talking about the same things here when they state "chronic fatigue" versus "chronic fatigue syndrome"?

Because if 20-30% of all adults had the level of impairment that many chronic Lyme disease patients have been diagnosed with - CFS - they would not be able to work.

Our economy would be in an even worse hole that it's been. I don't think their definition of chronic fatigue matches that which I observe in other chronic Lyme disease or PLDS patients.

And what is level 3 pain? Are they talking a "3" on a scale of 1-10? My pain has been much higher than that on numerous occasions.

Level 3. Is that it?

I would do a lot if I had level 3 pain all the time.

(Refer to Hyperbole and A Half's Pain Scale Post here.)

Regardless of this, I am concerned about the health of this country:

Why are so many adults fatigued and in pain? What is the etiology?

I don't remember people complaining of chronic fatigue when I was growing up. I don't remember talk about CFS until the 1980's, because it wasn't a diagnosis until then, anyway.

And I know a lot of people today and most of them do not complain about chronic fatigue - they are not on the couch or in bed most of the time.

They're out doing things, and then say they're tired after they've done them - not when they first wake up.

I think these guidelines do need rewriting, and while they are going to get an update in 2012, the proposed changes are so minor that they may get lost amid much of the verbiage.

Even so, I can't help but wonder if I will hear of any follow up on those late stage Lyme disease patients mentioned in trials in the 2000 guidelines - who at this point - may well have been suffering from treatment failures for over a decade.

Update:

This is what I get for initially writing this late at night. I went back to the guidelines and reread them to see if there was any update on some of these study participants. As it turns out, those who were in the longer term 143 patient multicenter study were followed up on later.

From the 2006 Guidelines:

"At time of the last evaluation, 5 patients in the 2-week treatment group had no apparent response to therapy, compared with none in the 4-week group (P = .07). The later the time point of evaluation, the higher the proportion of patients who were categorized as cured. A greater proportion of patients in the 4-week treatment group than in the 2-week group had therapy prematurely discontinued because of adverse events (P < .02). The principal conclusion of these 2 studies is that daily parenteral administration of ceftriaxone at a dosage of 2 g per day for 2 weeks is effective in resolving illness in the majority of patients with late Lyme disease. However, some patients have persistent symptoms despite receiving ceftriaxone treatment."

So some people did get better on their own after two weeks of IV antibiotics, but not everyone did. Some people continued to suffer with persisting symptoms.

More research is needed to find out why, and what can be done to help these people.

There is more I could say about sections of these guidelines, now that I've reread some of them - but that is for another post for another day.

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