Archive for the ‘Treatment’ Category

FREE: View “Under Our Skin” Best Primer on Lyme Disease

http://www.veoh.com/watch/v21055812yWtmpgB8  Approx. One hour forty five minutes.

If you have not watched the incredible documentary, “Under Our Skin,” please do so.  It reveals what patients and the doctors who dare to treat them go through.  It reveals the controversy up front and personally.  You will learn that Lyme is congenital, very probably a STD, and devastating.

The documentary covers so much ground but unfortunately doesn’t talk about the coinfections that typically come with Lyme (borrelia).

Artesunate on Short Term Memory in Lyme Borreliosis

http://www.medical-hypotheses.com/article/S0306-9877(17)30288-8/fulltext

Lyme borreliosis is associated with memory deficits. While this may be related to cerebral infection by Borrelia bacteria, it may also be caused by concomitant co-infection by Babesia protozoa. The anti-malarial artemisinin-derivative artesunate has been shown to be effective against a number of Babesia species and to have efficacy against human cerebral malaria. We hypothesised that concomitant administration of artesunate in Lyme borreliosis patients would help alleviate the severity of self-reported short-term memory impairment. This hypothesis was tested in a small pilot study in which patients were treated with both an intravenous antibiotic and oral artesunate (20 mg four times per day); treatment was associated with a reduction in the severity of short-term memory difficulties (P ≃ 0.08). In light of these findings, we recommend that a formal randomised, placebo-controlled study be carried out.

 

For more on Babesia:  https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/

More on Lyme:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

Busting Lyme Myths – NYC

Senator Sue Serino’s Lyme and Tick Borne Disease Forum 2017

NYC Senator, Sue Serino of the 41st District, is the Chair of the Senate’s Task Force on Lyme and TBIs.  Task Force members and state leaders in New York are holding awareness events across the state.  One event was a public forum, in the video above, busting prevalent myths surrounding all things TBI related.

Microbiologist Holly Ahern speaks first and educates the public on common Lyme and TBI myths.  Then Dr. Matt Frye, Integrative Pest Management IPM specialist, speaks on myths about ticks.

https://a.pgtb.me/tgZFPJ  Take a Bite Out of Lyme Disease website with more info.

**This is a fantastic talk full of great and accurate information.

My only possible disagreement is that Frye states ticks can not fall & bite from trees.  I’ve heard many patients swear (including the recent video I posted of TV anchor Mike Schneider) they were bit as they sat under a tree on a patio.  https://madisonarealymesupportgroup.com/2017/07/13/tv-anchor-speaks-out-about-lyme-disease/

Besides loving Japanese Barberries (shrub), https://madisonarealymesupportgroup.com/2015/09/30/barberry-friend-or-foe/  ticks at least here in Wisconsin love certain pine trees and I personally know of a family that would hang their laundry on a line outside where the clothes would gather ticks quite possibly from the pine trees that hung over top the line.  They would find the ticks when they dumped the laundry onto the bed.  Both the husband and wife become infected this way.

https://madisonarealymesupportgroup.com/2017/03/13/ticks-found-on-rocks/  This link reveals that ticks can show up in unexpected places like on top of rocks, under picnic tables, and on picnic benches.

As to trees and using logic, if birds and small rodents travel up and down trees 24/7, it only makes sense some are going to drop off and find a blood meal.

 

Mycoplasma and Other Intracellular Bacterial Infections in Rheumatic Diseases: Comorbid Condition or Cause?

https://www.peertechz.com/articles/mycoplasma-and-other-intracellular-bacterial-infections-in-rheumatic-diseases-comorbid-condition-or-cause.pdf  by Garth Nicolson, May, 2017  Open Journal of Tropical Medicine

Letter to the Editor

Although the causes of rheumatic diseases have remained relatively unknown, systemic intracellular bacterial infections are commonly found in rheumatic disease patients [1-4]. Because of this, certain infections have been confused with comorbid conditions.

Often patients with rheumatic diseases have co-morbidities, and some authors have concluded that this can include chronic infections. “Infections continue to be a significant cause of morbidity and mortality in patients with rheumatic diseases, and, consequently, early diagnosis and treatment of infection is critical to the successful medical management of these patients” [5].

A link between certain types of infections and rheumatic diseases has been seen by a number of authors. For example, infections with Mycoplasma species, Borrelia species and other intracellular bacteria have been linked to various forms of rheumatic disease [1-4, 6-13]. In addition, animal models of rheumatic disease have been established by infection with Mycoplasma species [13-15]. In one of these contributions experimental arthritis was induced by a clinical isolate from M. fermentans injected into the joints of rabbits [15]. Outbreaks of rheumatic disease, such as polyarthritis, have been traced to infections by Mycoplasma species [16]. Arthritis in animals caused by Mycoplasma species infections closely resemble the signs and symptoms found in patients with rheumatoid arthritis [17]. In addition, reactive arthritis following M. pneumonia infection has been seen in patients [18]. Mycoplasma infections have also been found in the joints of patients with rheumatic disease [19-21]. In a case-control study the presence of antibodies against Mycoplasma pneumoniae have been statistically correlated to the clinical features of rheumatoid arthritis (p<0.001) [21]. Furthermore, genetic analyses and transmission in animals indicate that arthritis is not directly linked to genetic abnormalities [22]. The pathogenesis of rheumatoid arthritis appears to be linked to immunological features of infection(s) involving host recognition of foreign antigens that mimic host antigens or host antigens that are incorporated into microorganism structures and the presence of localized immune complexes and the influences of environmental conditions [22].

Standard treatments of chronic infections like mycoplasma often employ long-term antibiotics, such as but not limited to tetracyclines and other antibiotics [23-26]. The U.S. National Institutes of Health sponsored a double-blind, placebocontrolled, long-term clinical trial that showed that the antibiotic minocycline was safe and effective for the treatment of rheumatoid arthritis. The antibiotic-treated patients showed greater improvements in joint swelling and tenderness (p<0.02), and the treatment group also had better improvements in hematocrit, SED rate, platelet counts and rheumatoid factor with no serious toxicity [27, 28]. A 4-year follow-up indicated that the minocycline-treated patients had fewer relapses and less frequent need for immune-suppressive drugs to control their RA (p<0.02) [29]. Although treatment of arthritis with antibiotics was effective and safe, treatment failures can, just as in any treatment for arthritis, be due to therapeutic failures, resistance and/or mutation of the microorganism [30].

Part of the reason that most rheumatic disease patients do not receive antibiotic treatment may have more to do with the enormous pressure from the marketing and sales of various drugs that do little to address the underlying causes of rheumatic diseases than the effectiveness of various treatments.

In summary, intracellular bacteria are commonly linked to rheumatic diseases, especially rheumatoid arthritis and similar conditions, and these infections can be successfully treated with antibiotics. Treatment often but not always resulted in significant reductions in rheumatic signs and symptoms. Thus chronic infections, such as intracellular bacterial infections, do not appear to be simply co-morbid conditions in rheumatic disease patients. Although there is circumstantial evidence, such as the animal transmission experiments discussed above, that infections like Mycoplasma species may be the cause of rheumatic diseases like rheumatoid arthritis, this has still not been conclusively proven in clinical cases.

References

1. Ford D (1991) The microbial causes of rheumatoid arthritis. J Rheumatol 18: 1441-1442. Link: https://goo.gl/NfKEJT

2. Krause A, Kamradt T, Burnmester GR (1996) Potential infectious agents in the induction of arthritides. Curr Opin Rheumatol 8: 203-209. Link: https://goo.gl/VNKX6m

3. Hyrich KL, Inman RD (2001) Infectious agents in chronic rheumatic diseases. Curr Opin Rheumatol 13: 300-304. Link: https://goo.gl/DekK3X

4. Horowitz S, Evinson B, Borer H, Horowitz J (2000) Mycoplasma fermentans in rheumatoid arthritis and other inflammatory arthritides. J Rheumatol 27: 2747-2753. Link: https://goo.gl/ysRguP

5. Segal BH, Sneller, MC (1997) Infectious complications of immunosuppressive therapy in patients with rheumatic diseases. Rheum Dis Clin North Amer 23: 219-237. Link: https://goo.gl/voNcLe

6. Ponka A (1979) Arthritis associated with Mycoplasma pneumoniae infection. Scand J Rheumato 8: 27-32. Link: https://goo.gl/G6iSdx

7. Schaeverbeke T, Vernhes JP, Lequen L, Bannwarth B, Bébéar C, et al. (1997) Mycoplasmas and arthritides. Rev Rheumatol Engl 64: 120-128. Link: https://goo.gl/bvdg2J

8. Schaeverbeke T, Gilroy CB, Bebear C, Dehais J, Taylor-Robinson D, et al. (1996) Mycoplasma fermentans but not M. penetrans detected by PCR in synovium from patients rheumatoid arthritis and other rheumatic disorders. J Clin Pathol 49: 824-828. Link: https://goo.gl/N6h76a

9. Hoffman RW, O’Sullivan FX, Schafermeyer KR, Moore TL, Roussell D, et al. (1997) Mycoplasma infection and rheumatoid arthritis analysis of their relationship using immunoblotting and an ultra-sensitive polymerase chain reaction detection method. Arthritis Rheumatol 40: 1219-1228. Link: https://goo.gl/YKeX8s

10. Haier J, Nasralla M, Franco AR, Nicolson GL (1999) Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatol 1999; 38: 504-509. Link: https://goo.gl/dgh5qA

11. Lünemann JD, Zarmas S, Priem S, Franz, J, Zschenderlein R, et al. (2001) Rapid typing of Borrelia burgdorferr sensu lato species in specimens from patients with different manifestations of Lyme Borreliosis. J Clin Microbiol 39: 1130-1133. Link: https://goo.gl/fDmCLr

12. Ford DK (1979) Yersinia-induced arthritis and Reiter’s syndrome. Ann Rheum Dis 38: 127-128. Link: https://goo.gl/d9xr2M

13. Cole BC, Griffi th MM (1993) Triggering and exacerbation of autoimmune arthritis by the Mycoplasma arthritidis super-antigen MAM. Arthritis Rheumatol 36: 994-1002. Link: https://goo.gl/SXre62

14. Mu HH, Nourian MM, Jiang HH, Justin WT, barry CC, et al. (2014) Mycoplasma super-antigen initiates a TLR4-dependent Th17 cascade that enhances arthritis after blocking B7-1 in Mycoplasma arthritidis-infected mice. Cell Microbiol 16: 896-911. Link: https://goo.gl/TzyHdX

15. Rivera A, Yanez A, Leon TG, Silvia G, Eduardo B, et al. (2002) Experimental arthritis induced by a clinical Mycoplasma fermentans isolate. BMC Musculoskelet Disord. Link: https://goo.gl/EQyzcM

16. Agnello S, Chetta M, Vicari Mancuso R, Manno C, Console A, et al. (2012) Severe outbreaks of polyarthritis in kids caused by Mycoplasma mycoides subspecies. Vet Rec. Link: https://goo.gl/x5mu4j

17. Jansson E, Backman A, Kakkarainen K, Miettinen A, Seniusová B (1983) Mycoplasmas and arthritis. Zeit Rheumatol 42: 315-319. Link: https://goo.gl/AYYBDt

18. Alvarez LB, Ceballos, BI, Alonso JL (2002) Reactive arthritis following a Mycoplasma infection. Med Clin (Barc).

19. Gilroy CB, Keat A, Taylor-Robinson D (2001) The prevalence of Mycoplasma fermentans in patients with infl ammatory arthritides. Rheumatol 40: 1355- 1358. Link: https://goo.gl/t6Vmgv

20. Ataee RA, Golmohammadi R, Alishiri GH, Esmaeili D, JonaidiJ, et al. (2015) Simultaneous detection of M. pneumoniae, M. hominis and M. arthritidis in snovial fl uid of patients with rheumatoid arthritis by multiplex PCR. Arch Iran Med 18: 345-350. Link: https://goo.gl/FQXsh3

21. Ramirez AS, Rosas A, Hernandez-Rerain JA, orengo JC, Saavedra P, et al. (2005) Relationship between rheumatoid arthritis and Mycoplasma pneumonia: a case-control study. Rheumatol 44: 912-914. Link: https://goo.gl/u9yq1Y

22. Ford DK (1969) Current views on the pathogenesis and etiology of rheumatoid arthritis. Canad Med Assoc 101: 147-151. Link: https://goo.gl/w2h9if

23. Nicolson GL, Nasralla M, Nicolson NL (1999) The pathogenesis and treatment of mycoplasma infections. Antimicrob Infect Dis Newsl 17: 81-88. Link: https://goo.gl/fGZz1S

24. Nicolson GL, Nasralla M, Franco AR, A. Robert F, Nancy LN, et al. (2000) Diagnosis and integrative treatment of intracellular bacterial infections in chronic fatigue and fi bromyalgia syndrome, Gulf War illness, rheumatoid arthritis and other chronic illnesses. Clin Pract Alt Med 1: 92-102. Link: https://goo.gl/YsX1mN

25. Baseman JB, Tully JG (1997) Mycoplasmas: sophisticated, reemerging and burdened by their notoriety. Emerg Infect Dis 3: 21-32. Link: https://goo.gl/rbHHgB

26. Couldwell DL, Lewis DA (2015) Mycoplasma genitalium infection: current treatment options, therapeutic failure and resistance-associated mutations. Infect Drug Resist 8: 147-161. Link: https://goo.gl/MxKQu8

27. Tilley BC, Alarcon GS, Heyse SP, David ET, Rosemarie N, et al. (1995) Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebocontrolled trial. MIRA Trial Group. Ann Intern Med 122: 81-89. Link: https://goo.gl/Hbh5jV

28. Pillemer SR, Fowler SE, Tilley BC, Graciela SA, Stephen P, et al. (1997) Meaningful improvement criteria sets in a rheumatoid arthritis clinical trial. MRIA Trial Group. Minocycline in rheumatoid arthritis. Arthritis Rheumatol 40: 419-425. Link: https://goo.gl/s8DXbf

29. O’Dell JR, Paulsen G, Haire CE, Kent B, William P, et al. (1999) Treatment of early sero-positive rheumatoid arthritis with minocycline: four year follow-up of a double-blind, placebo-controlled trial. Arthritis Rheumatol 42: 1691-1695. Link: https://goo.gl/G1jd4i

30. Razin S, Yogev D, Naot Y (1998) Molecular biology and pathogenicity of mycoplasmas. Microbiol Mol Biol Rev 62: 1094-1136. Link: https://goo.gl/tZBnMS

For more on Mycoplasma see: https://madisonarealymesupportgroup.com/2016/02/07/mycoplasma-treatment/

https://madisonarealymesupportgroup.com/2015/08/12/connecting-dots-mycoplasma/

https://madisonarealymesupportgroup.com/2017/07/14/clinical-association-lyme-disease-and-guillain-barre/

More on Minocycline:  https://madisonarealymesupportgroup.com/2017/06/04/minocycline-for-ms-and-much-more/

https://madisonarealymesupportgroup.com/2017/07/14/bells-palsy-despite-treatment/

Bell’s Palsy Despite Treatment

http://www.ijidonline.com/article/S1201-9712(17)30182-0/pdf

Progression of Lyme disease to Bell’s Palsy despite treatment with doxycycline

Luis A. Marcos, Zengmin Yan

International Journal of Infectious Diseases, online first July 10, 2017

Highlights

* Treatment of choice for Lyme disease remains controversial.
* Bell’s palsy developed despite being on doxycycline.
* Progression of disease may be related to a strong host immune response.
* Prompt clinical response to minocycline needs further investigation.

Abstract

A 54 year-old healthy woman presented to the emergency department with a right sided facial paralysis. About 3 weeks ago, she woke up and noticed an attached engorged tick in her right lower extremity. A week later, she noticed a mild to moderate right jaw pain which progressed to a severe right facial pain so she visited her doctor. On physical, II to XII cranial nerve examination was unremarkable.

Doppler ultrasound did not show any vascular abnormalities in temporal artery. Her inflammatory markers were within normal limits (C-reactive protein:0.3 mg/dL; sedimentation rate:6 mm/h). Further brain imaging by MRI reveled no abnormalities. Lyme serology (antibodies against purified VlsE-1 and PepC10 antigens) was negative (index value 0.6; ≤ 0.90 negative). Complete blood count and metabolic panel were within normal limits. Only objective physical finding was a right erythematous ear canal (red and inflamed) so the patient was prescribed a 7-day course of amoxicillin/clavulonic acid.

Two days later, the rash in right leg increase in size. It was described as 4 cm rash circular with erythematous edges, clearing and central erythema consistent with erythema migrans (EM) (bull’s eye). She was prescribed doxycycline 100 mg orally twice a day. Five days later went to see a neurologist due to worsening right facial shooting pain. Patient had minimal gastrointestinal side effects from the antibiotic and continued taking it every 12 hours without interruption. Physical exam revealed face symmetric, numbness in right chin in nerve distribution. She was diagnosed with possible Lyme cranial neuritis. Doxycycline was continued and pregabalin was started.

On day #10 of doxycycline, she woke up and noticed that her right face was paralyzed and unable to close the right eye so she went to the local emergency department. The EM was improved from 4 to 2 cm residual rash. Because of her headaches, a lumbar puncture and brain MRI were recommended. Cerebrospinal spinal fluid analysis revealed only 3 WBCs, protein 30.2 g/dL, glucose 62 mg/L, Lyme serology pair CSF fluid O.D. = 0.114 (borderline), serum Lyme serology pair O.D. = 0.409 (reactive), serum IgM western blot was positive (bands present: 23 and 41 kDa), serum IgG western blot was indeterminate (bands: 41,58 and 93 kDa), CRP remained less than 0.1 mg/dL. MRI of brain showed new increased enhancement involving right facial nerve.

She was discharged on minocycline 100 mg orally twice a day for 21 days. Two days later, her right side headaches improved significantly. The facial paralysis completely resolved after 1 week. At 3 months follow-up, she recovered completely without any complications.

**Lessons Learned**

*If you are bit by a tick, DO NOT WAIT AROUND!  Even the CDC is NOW stating suspected Tick borne illness to be treated empirically:  https://madisonarealymesupportgroup.com/2017/07/12/start-treatment-if-tbis-are-suspected/  That NEW official word has not reached the public or many main stream doctors so it’s up to you to educate people.

*The ER folks and her doctor had their heads in the sand.  When she presented with facial palsy and told them she was bit by a tick – BOOM – treatment should have started that very minute.  Do NOT wait around for lab results!

*Mainstream doctors will prescribe antibiotics for a possible ear infection, but they take a “wait and see” approach with Lyme disease.  Unfortunately amoxicillin isn’t a great drug for LD so it didn’t help this patient.  Few die of ear infections.  Many die of TBI’s.

*Doctors still follow the CDC’s ludicrous and arbitrary EM measurement.

*LD can progress to stage 3 (central nervous system involvement) quickly.  Here’s another case that literally went to stage 3 within hours:  https://madisonarealymesupportgroup.com/2016/12/07/igenex-presentation/

*Minocycline is a fantastic antibiotic that crosses the blood brain barrier:  https://madisonarealymesupportgroup.com/2017/06/04/minocycline-for-ms-and-much-more/

*Had the doctor and the ER treated her empirically, doxycycline probably would have done the job.

*This shows why doxy alone often doesn’t work.  Time is of the essence. 

*Hopefully this patient was not co-infected.  There is also the possibility of the non-cell wall form of borrelia to lie dormant to reemerge later.  The patient needs follow-up.

For more on Lyme disease treatment:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/