Clearly there are not a whole lot of details in the abstract. Got encephalitis or myelitis from a tick bite, it's obviously not Lyme, folks, it's gotta be Powassan. I must admit though, the last two sentences in this have me scratching my head. I am really puzzled as to why an 'asymptomatic' patient with IgG seropositivity would need 'appropriate management' and what research for this might entail. And, what the heck is an 'asymptomatic' erythema migrans skin rash and why would someone attribute a prior case of Lyme to something that had been overlooked?Wien Klin Wochenschr. 2016 Jan 14. [Epub ahead of print]
Management approaches for suspected and established Lyme disease used at the Lyme disease diagnostic center.
Wormser GP1, McKenna D2, Nowakowski J3.
2015 marks the 27th year that the Lyme Disease Diagnostic Center, located in New York State in the United States, has provided care for patients with suspected or established deer tick-transmitted infections. There are five deer tick-transmitted infectious in this geographic area of which Lyme disease is the most common.For patients with erythema migrans, we do not obtain any laboratory testing. However, if the patient is febrile at the time of the visit or reports rigors and high-grade fevers, we consider the possibility of a co-infection and order pertinent laboratory tests.Our preferred management for Lyme disease-related facial palsy and/or radiculopathy is a 2-week course of doxycycline. Patients who are hospitalized for Lyme meningitis are usually treated at least initially with ceftriaxone. We have not seen convincing cases of encephalitis or myelitis solely due to Borrelia burgdorferi infection in the absence of laboratory evidence of concomitant deer tick virus infection (Powassan virus). We have also never seen Lyme encephalopathy or a diffuse axonal peripheral neuropathy and suggest that these entities are either very rare or nonexistent.We have found that Lyme disease rarely presents with fever without other objective clinical manifestations. Prior cases attributed to Lyme disease may have overlooked an asymptomatic erythema migrans skin lesion or the diagnosis may have been based on nonspecific IgM seroreactivity. More research is needed on the appropriate management and significance of IgG seropositivity in asymptomatic patients who have no history of Lyme disease.
There are a few more excerpts courtesy of Rel-risk, (thank you, RR!) along with his usual biases which can be found just below: (In the spirit of 1984 - Everyone by now must know he has some kind of issue regarding poor, young, Afro-American men, right?)
http://rel-risk.blogspot.ca/2016/01/abs ... in-ld.html
Oh, good grief.......Here is a much earlier paper (from 1997) that begs to differ. It's pretty amazing that they reported such good results treating something that just doesn't exist. (Yup, I am just trying to get into 1984 spirit here, folks) Anyone want to be a fly on the wall when the two panel members for the 2015 Lyme guidelines (Wormser and Steere) hash this argument out?Sunday, January 17, 2016
Absent Entities in LD
Wormser GP, McKenna D, Nowakowski J. Management approaches for suspected and established Lyme disease used at the Lyme disease diagnostic center. Wien Klin Wochenschr. 2016 Jan 14.
2015 marks the 27th year that the Lyme Disease Diagnostic Center has provided care for patients with suspectedor established deer tick-transmitted infections. Located in the Lower Hudson Valley of New York State, this Center is run by an infectious diseases specialist and has served as a walk-in diagnostic, treatment and research facility for adults at least 18 years of age with tick bites or a clinical illness suspected to be transmitted by deer ticks.
We have seen various other manifestations of neurologic Lyme disease including other cranial nerve palsies and brachial plexopathy. However, we have not seen convincing cases of encephalitis or myelitis solely due to B. burgdorferi infection in the absence of laboratory evidence of concomitant deer tick virus infection (Powassan virus). It is possible that such cases do occur rarely, especially in Europe where they are likely associated with another species of Lyme Borrelia, namely B. garinii. While some patients with erythema migrans may complain of memory or concentration difficulties and these symptoms can persist for months to years in a small number of patients as a manifestation of post-treatment Lyme disease symptoms, we have never seen the poorly defined entity referred to as Lyme encephalopathy and question its existence. We also question the existence of a diffuse axonal peripheral neuropathy as a manifestation of Lyme disease, having never seen a bona fide case. Well-documented cases of a diffuse peripheral neuropathy also do not exist in Europe, to our knowledge, except in patients who manifest the late cutaneous manifestation of Lyme disease known as acrodermatitis chronica atrophicans; moreover, the peripheral neuropathy that occurs in patients with acrodermatitis chronica atrophicans is most often not diffuse but instead localized to the extremity manifesting the skin lesion.
Reasons why there could have been misdiagnoses leading to the perception of Lyme encephalopathy, or diffuse peripheral neuropathy, and/or other unusual manifestations of Lyme disease, is the relatively high frequency of positive Lyme disease serologic tests in certain populations, either due to false-positive test reactivity (especially with earlier testing methods), a prior diagnosed, treated, and resolved case of Lyme disease, an asymptomatic latent infection or a spontaneously resolved infection. Whenever a positive test is found the clinician is faced with the critical question of whether the results are related or unrelated to the patient’s clinical picture. An alternative explanation is that encephalomyelitis, Lyme encephalopathy and diffuse peripheral neuropathy are extremely rare, or are caused by Lyme Borrelia strains not found in our geographic area.
Disturbing news to the many online Lyme activists: some of their symptoms have nothing to do with Lyme disease. Still, that hasn’t stopped one well-known activist from reading the abstract to the above paper and declaring:
“THIS is one of the reasons we have over 25 THOUSAND members here. They weren't cured using the 2 weeks of doxy theory! They are trying to kill us all!”
Yes, it’s a fiendish conspiracy to reduce the population of white, middle-aged women with nonspecific, subjective complaints of pain, discomfort and depression. Of course, this same nut insisted in 2011 that she was infected with 13 different bacteria, viruses, and parasites. Not even the mangiest mutt in India or Egypt or South Africa would be so burdened. But then it’s hard to tell crazy people that they’re crazy.
Successful Treatment of Lyme Encephalopathy with Intravenous Ceftriaxone
Eric L. Logigian1,4,a, Richard F. Kaplan1,2,a and Allen C. Steere2,3
The efficacy of intravenous ceftriaxone, 2 g per day for 30 days, was evaluated in a case series of 18 consecutive patients who met strict criteria for Lyme encephalopathy. Months to years after classic manifestations of Lyme disease, the 18 patients presented with memory difficulty, minor depression, somnolence, or headache. Sixteen (89%) had abnormal memory scores; 16 (89%) had cerebrospinal fluid (CSF) abnormalities, and all 7 patients tested had frontotemporal perfusion defects on single photon emission computed tomographic (SPECT) imaging. Six months after treatment, memory scores in the 15 patients who completed the study according to protocol were significantly improved (P < .01). In the 10 patients who had follow-up CSF analyses, total protein levels were significantly lower (P < .05). In the 7 patients who had SPECT imaging, posttreatment perfusion was significantly better (P < .01). Twelve to 24 months after treatment, all 18 patients rated themselves as back to normal or improved. We conclude that Lyme encephalopathy can be treated successfully with ceftriaxone.