An article was written recently that supposedly contained “9 myths about lyme disease”. That article can be found here: http://www.huffingtonpost.com/2013/05/20/lyme-disease-myths-facts_n_3287872.html?utm_hp_ref=email_share
Dr. Maloney critiques the article on Facebook, but I’ll include it here so that I can look back on it before it rolls off of the Facebook timeline:
As a physician who writes accredited evidence-based educational courses and publishes on Lyme, I noted several factual mistakes in this well-meaning article.
1. The 30,000 reported cases are those meeting a rigid surveillance case definition (SDC) developed by public health officials to track disease. Their narrow definition allows them to avoid tracking someone who doesn’t have Lyme. The SCD does not include well-known neurological manifestations of Lyme disease such as encephalopathy. It requires that patients have positive results on antibody testing, with criteria for a “positive test” also being narrowly defined. Although counter-intuitive, reportable cases are not usually reported; somewhere between 2/3 and 11/12 go unreported.
Clinicians care for the sick and therefore use broader disease definitions. They recognize the consequences of missing Lyme disease. While cognizant of the need to avoid “seeing Lyme everywhere” , they know if a diagnostic error is to be made, better to over-diagnose than under-diagnose. Dr. Mead’s 2004 testimony to state officials in CT made that very point. Some clinicians understand that in patients with an exposure history to black-legged ticks, symptoms and findings compatible with Lyme disease and no other likely explanations for their clinical manifestations, it is entirely appropriate to make a clinical diagnosis of Lyme disease and move forward, whether or not testing confirms the infection. Should the diagnosis be incorrect, this will become apparent during follow-up, when the expected antibiotic effect is missing.
2. In areas where Lyme is highly endemic, the infection rate in local tick populations is much higher than Dr. Mead’s suggestion of 1 out of 4 or 5. In popular vacation areas of MN, 2/3 ticks are infected.
3. Although not part of the article, it should be noted that these ticks carry other agents of disease, including Anaplasma, Babesia, Ehrlichia muris-like agents, Borrelia miyamotoi (related to the Lyme bacteria Borrelia burgdorferi) , viruses and probably species of Bartonella bacteria. A single bite can transmit multiple infectious agents and having co-infections complicates diagnosis and treatment.
4. According to 15 years of CDC surveillance data, roughly 70% of case reports noted the presence of an EM rash. A recent study found the likelihood of developing a rash depended on which species and strain of the bacteria caused the infection.
The classic “bull&# 39;s-eye” rash is seen in < 20% of all rashes. Thus, patients with early disease are more likely to have no rash than to have a bull’s-eye.
5. The list of neurologic problems secondary to Lyme is much more extensive than Dr. Mead suggests and is well-documented in the literature.
6. The comments regarding persist disease – lingering or progressive symptoms and findings – seem to minimize the possibility of persistent infection. This is a mistake as persistent infection in humans is well-documented in the literature and several animal studies, using a wide variety of animal species, demonstrated persistent infection is not a fluke occurrence. Interested readers should check out studies by Embers, Barthold and Hodzic.
One of the few studies of late neurologic disease (Logigian E) noted that peripheral nervous system findings in his subjects occurred an average of 16 months post-rash and central nervous system changes were seen 26 months post-rash. These findings were typically accompanied by systemic symptoms like fatigue, sleep disorders, cognitive problems.
Given that direct evidence of the bacteria’ s presence is rarely demonstrated prior to treatment, it is unrealistic to require such proof post-therapy in order to conclude that persistent disease is due to persistent infection. As an epidemiologist and not a clinician, Dr. Mead may not realize that his broken bone analogy is flawed. In some fractures, failure to heal (known as non-union), is quite common.
Which isn’t to say that there aren’t other potential mechanisms but certainly none have been as well demonstrated as persistent infection.
7. Dr. Mead’s comments about treating persistent symptoms represent the conventional medical wisdom but he should know better. Last fall two separate papers, including one by Allison Delong that I co-authored, carefully reviewed the 4 NIH-sponsored trials and demonstrated that in 2 trials, IV antibiotic re-treatment resulted in clinically meaningful improvements in patients with severe fatigue. Unfortunately, the risk of adverse events was significant. But patients with disabling fatigue like that seen in these 2 studies, may determine that the potential benefits justified the risk. Hopefully new research will identify other patient subgroups that would also benefit from antibiotic re-treatment as well as antibiotic protocols that are equally, or more, effective and less likely to cause problems. That won’t happen if members of the CDC’s Lyme program have already given up on this line of therapy.
8. Testing is not reliable and definitely cannot rule out disease. Common blood tests look for antibodies that can take weeks for the body to produce, which is why testing during the rash phase is discouraged.
Once produced, levels do not necessarily remain high in people who are infected. The bacteria are a zoonotic pathogen, able to survive in multiple animal species – ticks, lizards, mammals and birds. To do this it must be able to adapt to these different hosts, including the host’s immune response. Thus, it has developed ways to evade the immune system and after a time antibody production decreases because the body isn’t “seeing” the bacteria. In a 1999 study by Logigian, where subjects absolutely had to have evidence of Lyme to be included, 17% lacked positive serology. In Embers 2012 monkey trial, antibody levels as measured by the C6 ELISA, declined after treatment even though the animals had evidence of persistent infection on autopsy. Even more interesting is the fact that 50%of the untreated animals also had their antibody levels drop back to normal as time went by. This has real implications for patients with late neurologic disease because they often experience diagnostic delays of several years and with the passage of time they are even less like to be diagnosed if it requires a positive blood test.
9. There is one well documented route of human to human transmission – in utero.
A lot of discussion is going on right now between doctors and researchers. It will be interesting to see how it all pans out in the end!