Archive for the ‘Bartonella’ Category

Four Essential Oils for Stopping Bartonella From Taking Over Your Brain

Four Essential Oils for Stopping Bartonella from Taking Over Your Brain

lavaPublished on October 30, 2018

Greg Lee (Founder of the Two Frogs Healing Center)

For people with neurological Bartonella symptoms of swelling and anxiety

My nephew invited us to his wedding in Hawaii. As we were booking our trip, the Kilauea volcano started spewing lava into residential neighborhoods. People had no other choice and had to evacuate as their homes and cars were burned by the spreading lava.

How is flowing lava similar to neurological Bartonella infections in people with Lyme disease?

Just like a hot lava eruption, a Bartonella infection can slowly burn through your body

Bartonella is a rod shaped, gram-negative bacteria that can be transmitted to humans via insect bites1, animal scratches and bites2, organ transplant3, needle sticks4, and blood transfusion5. At least thirteen different species of Bartonella are known to infect humans6. Bartonella has been shown to infect endothelial cells, macrophages, red blood cells7, and the lymphatic system8. Bartonella can spread through the bloodstream via the lymphatic system9. Bartonella manipulates the production of vascular endothelial growth factor10 (VEGF) and Interleukin-811 (IL-8) to make it easier for it to spread via new blood vessels through the skin and the body. Unfortunately, Bartonella can also infect the nervous system.

Bartonella has been detected in the cerebral spinal fluid of patients12

Patients with a Bartonella infection may present with multiple neurological symptoms including: confusion, encephalitis13, vision loss, neuroretinitis, optic neuropathy14, subarachnoid hemorrhage, cerebral embolism15, fever, vomiting, ataxia16, slurred speech, weakness17, convulsions18, chronic inflammatory demyelinating polyneuropathy19, depression, anxiety, mood swings, severe headaches, muscle spasms, decreased peripheral vision, diminished tactile sensation, and hallucinations20. Multiple patients have both Bartonella and Lyme disease in their nervous system21. Inflammation may play a role in Bartonella’s ability to spread into the brain.

Inflammatory compounds may help Bartonella spread into the nervous system

Patients diagnosed with Bartonella have elevated levels of IL-822, Interleukin-1023 (IL-10), and vascular endothelial growth factor24 (VEGF). Elevated levels of IL-825 and VEGF26 have been correlated with blood brain barrier increased permeability and dysfunction. Il-10 may help to protect the blood brain barrier27. Similarly, inflammatory compounds Interleukin-6 (IL-6), Interleukin- (IL-8), chemokine ligand 2 (CCL2), and CXCL13 are implicated in the spread of Lyme disease in the nervous system28. Another factor in persistent neurological infections may be due to drug resistant Bartonella strains that have been discovered.

Bartonella drug resistant strains have been discovered

Highly antibiotic resistant mutants of Bartonella bacilliformis have been found in a lab study29. Another study has found drug resistant forms of Bartonella henselae30.

Can essential oils help to reduce recurring neurological symptoms by preventing how Bartonella may spread into the nervous system?

Fortunately, there are four essential oils that lower the inflammatory compounds that Bartonella uses to spread through the body

In multiple studies, essential oils were effective at lowering inflammatory compounds and symptoms like anxiety that may be elevated in neurological Bartonella infections. Formulating these oils into microparticles called liposomes may help deliver these remedies deeper inside the brain. Many of these essential oils have been used safely for years in our food supply31. Formulating these essential oils into microparticles called liposomes may help them penetrate deeper inside of blood cells, endothelial cells and the nervous system where Bartonella likes to hide32.

Anti-Neurological Bartonella Essential Oil #1: Peppermint

In a mouse wound study, peppermint essential oil was effective at lowering VEGF and increasing IL-1033. Peppermint oil has had positive effects in reducing anxiety in human studies34. Do not apply peppermint oil undiluted to the feet of children under 12 years old, avoid large doses, it may cause heartburn, perianal burning, blurred vision, nausea and vomiting when taken internally. Peppermint essential oil use is contraindicated in children under 30 months old, and people should avoid the intake of peppermint oil with gallbladder disease, severe liver damage, gallstones, chronic heartburn35, and cases of cardiac fibrillation and in patients with a G6PD (Glucose-6-Phosphate Dehydrogenase) deficiency36. This oil is classified as Generally Recognized as Safe (GRAS) by the FDA37. Black cumin seed oil may also help to lower VEGF.

Anti-Neurological Bartonella Essential Oil #2: Black Cumin Seed

In lab studies, black cumin seed oil down regulated the expression of VEGF in endothelial cells38. In a rat study, this oil increased levels of tryptophan and reduced anxiety levels39. Black cumin seed oil is contraindicated in pregnancy and breastfeeding. It’s use is cautioned with diabetes medications, on hypersensitive, diseased or damaged skin, and in children under 2 years of age40. Mastic gum essential oil also lowers VEGF in experiments.

Anti-Neurological Bartonella Essential Oil #3: Mastic Gum

In a mouse lab study, mastic essential oil inhibited the release of VEGF41. In an outpatient study on Crohn’s disease, mastic gum decreased IL-6 and C-reactive protein (CRP)42. Citron essential oils lowered VEGF in a lab study.

Anti-Neurological Bartonella Essential Oil #4: Citron

In a lab study, citron essential oil lowered VEGF in endothelial cells43. These essential oils alone or in combination may help to reduce neurological symptoms caused by a spreading Bartonella infection in the nervous system.

Essential oils may help to reduce the spread of inflammation caused by neurological Bartonella infection

Similar to lava that is stopped by the cold waters of the ocean, essential oils that lower Bartonella inflammatory compounds may limit it’s spread in the brain and reduce neurological symptoms. Formulating these essential oils into microparticle liposomes may enhance their ability to penetrate into cells and stop Bartonella from invading the nervous system. Since these essential oils have cautions and contraindications on their use, work with a Lyme literate essential oil practitioner to develop a proper, safe, and effective strategy for your condition.

1 Billeter, S. A., M. G. Levy, B. B. Chomel, and E. B. Breitschwerdt. “Vector Transmission of Bartonella Species with Emphasis on the Potential for Tick Transmission.” Medical and Veterinary Entomology 22, no. 1 (March 2008): 1–15. https://doi.org/10.1111/j.1365-2915.2008.00713.x.

2 “Transmission | Bartonella | CDC.” Accessed July 22, 2016.http://www.cdc.gov/bartonella/transmission/.

3 Scolfaro, C., F. Mignone, F. Gennari, A. Alfarano, A. Veltri, R. Romagnoli, and M. Salizzoni. “Possible Donor-Recipient Bartonellosis Transmission in a Pediatric Liver Transplant.” Transplant Infectious Disease: An Official Journal of the Transplantation Society 10, no. 6 (December 2008): 431–33.https://doi.org/10.1111/j.1399-3062.2008.00326.x.

4 Breitschwerdt, Edward Bealmear. “Bartonellosis: One Health Perspectives for an Emerging Infectious Disease.” ILAR Journal 55, no. 1 (2014): 46–58. https://doi.org/10.1093/ilar/ilu015.

5 Núñez, M. Antonieta, Karla Contreras, M. Soledad Depix, Enrique Geoffroy, Nicolás Villagra, Sandra Mellado, and Ana M. Salinas. “[Prevalence of Bartonella henselae in blood donors and risk of blood transmission in Chile].” Revista Chilena De Infectologia: Organo Oficial De La Sociedad Chilena De Infectologia 34, no. 6 (December 2017): 539–43. https://doi.org/10.4067/S0716-10182017000600539.

6 Lamas, C., A. Curi, Mn Bóia, and Ers Lemos. “Human Bartonellosis: Seroepidemiological and Clinical Features with an Emphasis on Data from Brazil – a Review.” Memorias Do Instituto Oswaldo Cruz 103, no. 3 (May 2008): 221–35.

7 Breitschwerdt, Edward Bealmear. “Bartonellosis: One Health Perspectives for an Emerging Infectious Disease.” ILAR Journal 55, no. 1 (2014): 46–58. https://doi.org/10.1093/ilar/ilu015.

8 Choi, Alexander H., Michael Bolaris, Diana K. Nguyen, Eduard H. Panosyan, Joseph L. Lasky, and Gloria B. Duane. “Clinicocytopathologic Correlation in an Atypical Presentation of Lymphadenopathy with Review of Literature.” American Journal of Clinical Pathology 143, no. 5 (May 2015): 749–54.https://doi.org/10.1309/AJCPPSKWRX0GD8HJ.

9 Hong, Jiehua, Yan Li, Xiuguo Hua, Yajie Bai, Chunyan Wang, Caixia Zhu, Yuming Du, Zhibiao Yang, and Congli Yuan. “Lymphatic Circulation Disseminates Bartonella Infection Into Bloodstream.” The Journal of Infectious Diseases 215, no. 2 (January 15, 2017): 303–11. https://doi.org/10.1093/infdis/jiw526.

10 Kempf, V. A., B. Volkmann, M. Schaller, C. A. Sander, K. Alitalo, T. Riess, and I. B. Autenrieth. “Evidence of a Leading Role for VEGF in Bartonella Henselae-Induced Endothelial Cell Proliferations.”Cellular Microbiology 3, no. 9 (September 2001): 623–32.

11 McCord, Amy M., Sandra I. Resto-Ruiz, and Burt E. Anderson. “Autocrine Role for Interleukin-8 in Bartonella Henselae-Induced Angiogenesis.” Infection and Immunity 74, no. 9 (September 2006): 5185–90.https://doi.org/10.1128/IAI.00622-06.

12 Samarkos, Michael, Vasiliki Antoniadou, Aristeidis G. Vaiopoulos, and Mina Psichogiou. “Encephalopathy in an Adult with Cat-Scratch Disease.” BMJ Case Reports 2018 (March 5, 2018).https://doi.org/10.1136/bcr-2017-223647.

13 Samarkos, Michael, Vasiliki Antoniadou, Aristeidis G. Vaiopoulos, and Mina Psichogiou. “Encephalopathy in an Adult with Cat-Scratch Disease.” BMJ Case Reports 2018 (March 5, 2018).https://doi.org/10.1136/bcr-2017-223647.

14 Habot-Wilner, Zohar, Omer Trivizki, Michaella Goldstein, Anat Kesler, Shiri Shulman, Josepha Horowitz, Radgonde Amer, et al. “Cat-Scratch Disease: Ocular Manifestations and Treatment Outcome.” Acta Ophthalmologica, March 5, 2018. https://doi.org/10.1111/aos.13684.

15 Yuan, Y., M. Shen, and X. G. Gao. “[Presented with subarachnoid hemorrhage and then blood culture negative infective endocarditis: a case report and literature review].” Beijing Da Xue Xue Bao. Yi Xue Ban = Journal of Peking University. Health Sciences 49, no. 6 (December 18, 2017): 1081–86.

16 Barnafi, Natalia, Natalia Conca, Cecilia von Borries, Isabel Fuentes, Francisca Montoya, and Elisa Alcalde. “[Central nervous system infection by Bartonella henselae associated with a choroid plexus papilloma].” Revista Chilena De Infectologia: Organo Oficial De La Sociedad Chilena De Infectologia 34, no. 4 (August 2017): 383–88. https://doi.org/10.4067/s0716-10182017000400383.

17 Teoh, Laurence S G, Hamish H Hart, May Ching Soh, Jonathan P Christiansen, Hasan Bhally, Martin S Philips, and Dominic S Rai-Chaudhuri. “Bartonella Henselae Aortic Valve Endocarditis Mimicking Systemic Vasculitis.” BMJ Case Reports 2010 (October 21, 2010). https://doi.org/10.1136/bcr.04.2010.2945.

18 Balakrishnan, Nandhakumar, Marna Ericson, Ricardo Maggi, and Edward B. Breitschwerdt. “Vasculitis, Cerebral Infarction and Persistent Bartonella Henselae Infection in a Child.” Parasites & Vectors 9, no. 1 (2016): 254. https://doi.org/10.1186/s13071-016-1547-9.

19 Mascarelli, Patricia E, Ricardo G Maggi, Sarah Hopkins, B Robert Mozayeni, Chelsea L Trull, Julie M Bradley, Barbara C Hegarty, and Edward B Breitschwerdt. “Bartonella Henselae Infection in a Family Experiencing Neurological and Neurocognitive Abnormalities after Woodlouse Hunter Spider Bites.”Parasites & Vectors 6 (April 15, 2013): 98. https://doi.org/10.1186/1756-3305-6-98.

20 Breitschwerdt, Edward B., Patricia E. Mascarelli, Lori A. Schweickert, Ricardo G. Maggi, Barbara C. Hegarty, Julie M. Bradley, and Christopher W. Woods. “Hallucinations, Sensory Neuropathy, and Peripheral Visual Deficits in a Young Woman Infected with Bartonella Koehlerae ▿.” Journal of Clinical Microbiology49, no. 9 (September 2011): 3415–17. https://doi.org/10.1128/JCM.00833-11.

21 Podsiadły, Edyta, Tomasz Chmielewski, and Stanisława Tylewska-Wierzbanowska. “Bartonella Henselae and Borrelia Burgdorferi Infections of the Central Nervous System.” Annals of the New York Academy of Sciences 990 (June 2003): 404–6.

22 McCord, Amy M., Sandra I. Resto-Ruiz, and Burt E. Anderson. “Autocrine Role for Interleukin-8 in Bartonella Henselae-Induced Angiogenesis.” Infection and Immunity 74, no. 9 (September 2006): 5185–90.https://doi.org/10.1128/IAI.00622-06.

23 Huarcaya, Erick, Ciro Maguina, Ivan Best, Nelson Solorzano, and Lawrence Leeman. “Immunological Response in Cases of Complicated and Uncomplicated Bartonellosis during Pregnancy.” Revista Do Instituto De Medicina Tropical De Sao Paulo 49, no. 5 (October 2007): 335–37.

24 Kempf, V. A., B. Volkmann, M. Schaller, C. A. Sander, K. Alitalo, T. Riess, and I. B. Autenrieth. “Evidence of a Leading Role for VEGF in Bartonella Henselae-Induced Endothelial Cell Proliferations.”Cellular Microbiology 3, no. 9 (September 2001): 623–32.

25 Kossmann, T., P. F. Stahel, P. M. Lenzlinger, H. Redl, R. W. Dubs, O. Trentz, G. Schlag, and M. C. Morganti-Kossmann. “Interleukin-8 Released into the Cerebrospinal Fluid after Brain Injury Is Associated with Blood-Brain Barrier Dysfunction and Nerve Growth Factor Production.” Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism 17, no. 3 (March 1997): 280–89. https://doi.org/10.1097/00004647-199703000-00005.

26 Zhang, Zheng Gang, Li Zhang, Quan Jiang, Ruilan Zhang, Kenneth Davies, Cecylia Powers, Nicholas van Bruggen, and Michael Chopp. “VEGF Enhances Angiogenesis and Promotes Blood-Brain Barrier Leakage in the Ischemic Brain.” Journal of Clinical Investigation 106, no. 7 (October 1, 2000): 829–38.

27 Lin, Ronggui, Fei Chen, Shi Wen, Tianhong Teng, Yu Pan, and Heguang Huang. “Interleukin-10 Attenuates Impairment of the Blood-Brain Barrier in a Severe Acute Pancreatitis Rat Model.” Journal of Inflammation (London, England) 15 (2018): 4. https://doi.org/10.1186/s12950-018-0180-0.

28 Ramesh, Geeta, Peter J. Didier, John D. England, Lenay Santana-Gould, Lara A. Doyle-Meyers, Dale S. Martin, Mary B. Jacobs, and Mario T. Philipp. “Inflammation in the Pathogenesis of Lyme Neuroborreliosis.”The American Journal of Pathology 185, no. 5 (May 2015): 1344–60.https://doi.org/10.1016/j.ajpath.2015.01.024.

29 Gomes, Cláudia, Sandra Martínez-Puchol, Lidia Ruiz-Roldán, Maria J. Pons, Juana del Valle Mendoza, and Joaquim Ruiz. “Development and Characterisation of Highly Antibiotic Resistant Bartonella BacilliformisMutants.” Scientific Reports 6 (September 26, 2016): 33584. https://doi.org/10.1038/srep33584.

30 Biswas, Silpak, Ricardo G. Maggi, Mark G. Papich, and Edward B. Breitschwerdt. “Molecular Mechanisms of Bartonella Henselae Resistance to Azithromycin, Pradofloxacin and Enrofloxacin.” Journal of Antimicrobial Chemotherapy 65, no. 3 (March 1, 2010): 581–82. https://doi.org/10.1093/jac/dkp459.

31 Hyldgaard, Morten, Tina Mygind, and Rikke Louise Meyer. “Essential Oils in Food Preservation: Mode of Action, Synergies, and Interactions with Food Matrix Components.” Frontiers in Microbiology 3 (January 25, 2012). https://doi.org/10.3389/fmicb.2012.00012.

32 Sherry, Mirna, Catherine Charcosset, Hatem Fessi, and Hélène Greige-Gerges. “Essential Oils Encapsulated in Liposomes: A Review.” Journal of Liposome Research 23, no. 4 (December 2013): 268–75.https://doi.org/10.3109/08982104.2013.819888.

33 Modarresi, Mohammad, Mohammad-Reza Farahpour, and Behzad Baradaran. “Topical Application of Mentha Piperita Essential Oil Accelerates Wound Healing in Infected Mice Model.” Inflammopharmacology, July 6, 2018. https://doi.org/10.1007/s10787-018-0510-0.

34 Stea, Susanna, Alina Beraudi, and Dalila De Pasquale. “Essential Oils for Complementary Treatment of Surgical Patients: State of the Art.” Evidence-Based Complementary and Alternative Medicine : ECAM 2014 (2014). https://doi.org/10.1155/2014/726341.

35 “Peppermint Safety Info | National Association for Holistic Aromatherapy.” Accessed April 1, 2017. http://naha.org/naha-blog/peppermint-safety-info/.

36 Tisserand, Robert, and Rodney Young. Essential Oil Safety: A Guide for Health Care Professionals. 2 edition. Edinburgh: Churchill Livingstone, 2013.

37 “CFR – Code of Federal Regulations Title 21.” Accessed October 28, 2018.https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=182.20.

38 M. Baharetha, Hussein, Zeyad Nassar, Abdalrahim Aisha, Abd Kadir M.O, Zhari Ismail, and Amin Malik Shah Abdul Majid. “Essential Oil of Nigella Sativa Inhibits Angiogenesis via Down-Regulation of VEGF Expression,” 2015. https://doi.org/10.4172/2375-4273.C1.009.

39 Perveen, Tahira, Saida Haider, Sumera Kanwal, and Darakhshan Jabeen Haleem. “Repeated Administration of Nigella Sativa Decreases 5-HT Turnover and Produces Anxiolytic Effects in Rats.”Pakistan Journal of Pharmaceutical Sciences 22, no. 2 (April 2009): 139–44.

40 Tisserand, Robert, and Rodney Young. Essential Oil Safety: A Guide for Health Care Professionals. 2 edition. Edinburgh: Churchill Livingstone, 2013. p. 793.

41 Loutrari, Heleni, Sophia Magkouta, Anastasia Pyriochou, Vasiliki Koika, Fragiskos N. Kolisis, Andreas Papapetropoulos, and Charis Roussos. “Mastic Oil from Pistacia Lentiscus Var. Chia Inhibits Growth and Survival of Human K562 Leukemia Cells and Attenuates Angiogenesis.” Nutrition and Cancer 55, no. 1 (2006): 86–93. https://doi.org/10.1207/s15327914nc5501_11.

42 Kaliora, Andriana C, Maria G Stathopoulou, John K Triantafillidis, George VZ Dedoussis, and Nikolaos K Andrikopoulos. “Chios Mastic Treatment of Patients with Active Crohn’s Disease.” World Journal of Gastroenterology : WJG 13, no. 5 (February 7, 2007): 748–53. https://doi.org/10.3748/wjg.v13.i5.748.

43 “Effects of Citron Essential Oils on Normal Human Epidermal Keratinocytes Stimulated with Vitamin D3 and TNF-A.” Journal of the American Academy of Dermatology 76, no. 6 (June 1, 2017): AB110.https://doi.org/10.1016/j.jaad.2017.04.436.

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For more on essential oils:  https://madisonarealymesupportgroup.com/2017/10/13/oregano-cinnamon-and-clove-found-to-have-high-anti-persister-activity-for-bb/

https://madisonarealymesupportgroup.com/2018/10/26/essential-oils-as-treatment-against-lyme-disease/

https://madisonarealymesupportgroup.com/2018/08/02/can-these-essential-oils-help-lyme-patients-overcome-chronic-candida/

I have personally used 1-2 drops of DMSO in a capsule with EO’s instead of the liposomal form with success.  I can smell/taste the DMSO so I know even at that low dose it’s gone systemic, driving the EO’s deep into the body, yet, it can’t be smelled by others at this dose!  Also, I use black seed oil as a carrier as well, which is listed as #2 in the article.  If you haven’t read about the usage of DMSO, please go here and learn:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

More on Bartonella treatment:  https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/

 

Category:

Bartonella, Herbs, Inflammation, Psychological Aspects, research, Treatment

Prophage-driven Genomic Structural Changes Promote Bartonella Vertical Evolution

https://www.ncbi.nlm.nih.gov/m/pubmed/30346520/

Prophage-driven genomic structural changes promote Bartonella vertical evolution

Ricardo Gutiérrez, Barak Markus, Keyla Carstens, Marques de Sousa, Evgeniya Marcos-Hadad, Raja C Mugasimangalam, Yaarit Nachum-Biala, Hadas Hawlena, Shay Covo, Shimon Harrus
Genome Biology and Evolution, evy236, https://doi.org/10.1093/gbe/evy236
22 October 2018

Abstract

Bartonella is a genetically diverse group of vector-borne bacteria. Over 40 species have been characterized to date, mainly from mammalian reservoirs and arthropod vectors. Rodent reservoirs harbor one of the largest Bartonella diversity described to date, and novel species and genetic variants are continuously identified from these hosts. Yet, it is still unknown if this significant genetic diversity stems from adaptation to different niches or from intrinsic high mutation rates. Here, we explored the vertical occurrence of spontaneous genomic alterations in 18 lines derived from two rodent-associated Bartonella elizabethae-like strains, evolved in non-selective agar plates under conditions mimicking their vector- and mammalian-associated temperatures, and the transmission cycles between them (i.e. 26 °C, 37 °C, and alterations between the two), using mutation accumulation experiments.

After ∼1000 generations, evolved genomes revealed few point mutations (average of one-point mutation per line), evidencing conserved single-nucleotide mutation rates. Interestingly, three large structural genomic changes (two large deletions and an inversion) were identified over all lines, associated with prophages and surface adhesin genes. Particularly, a prophage, deleted during constant propagation at 37 °C, was associated with an increased autonomous replication at 26 °C (the flea-associated temperature). Complementary molecular analyses of wild strains, isolated from desert rodents and their fleas, further supported the occurrence of structural genomic variations and prophage-associated deletions in nature. Our findings suggest that structural genomic changes represent an effective intrinsic mechanism to generate diversity in slow-growing bacteria and emphasize the role of prophages as promoters of diversity in nature.

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**Comment**

Bacteriophages or simply phages were discovered in the early 1900’s and are viruses which infect a bacterium causing horizontal gene transfer which in turn causes bacterial evolution.  

If you don’t know it yet, what goes into a Lyme/MSIDS patient is not what comes out.  These critters morph inside us turning into something quite different, which is one reason this complex is so difficult to treat.

When I read a book on antibiotic resistance, thankfully something that is not occurring yet in Lyme/MSIDS with few exceptions, I learned of phage therapy.  If this interests you check this out (located in the Republic of Georgia):  https://www.phagetherapycenter.com/pii/PatientServlet?command=static_phagetherapy

News articles on phage therapy:  https://www.phagetherapycenter.com/pii/PatientServlet?command=static_news&secnavpos=4&language=0

I’ve been told phage therapy wouldn’t work with Lyme/MSIDS due to the lack of host specificity.  In other words, the phage must directly line up with the specific bacteria in order to work.  Also, most of us are dealing with more than one bacteria, and battle worms, parasites, and other lovely beasts thrown into the mix to keep us humble.

The take home from this abstract is that the bacteria we are infected with are intelligent and stealthy, changing within us to further their goals.  They don’t want to kill us, just maim and weaken us so they can live long, full lives.  Also, notice “slow-growing bacteria,” which should serve as a clue to practitioners that these types of organisms scoff at 21 days of antibiotics.

Category:

Bartonella, Viruses

Skull Infection Due to Bartonella

https://www.ncbi.nlm.nih.gov/m/pubmed/30319958/

Skull osteomyelitis as a rare complication of cat scratch disease.

Rafee Y, et al. Avicenna J Med. 2018 Oct-Dec.

Abstract

Bartonella henselae, the causative agent of cat scratch disease (CSD), is one of the most common causes of regional lymphadenitis in children. Other less common manifestations of B. henselae infection including fever of unknown origin, neuroretinitis, and osteomyelitis are being increasingly recognized. We describe a 3-year-old female with a recent history of typical CSD involving lymph nodes who developed osteomyelitis of the skull, a very rarely recognized complication of this infection.

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**Comment**

Having spent two days getting my head crammed full of information on Bartonella from some of the leading experts, I chuckle once again at the words, “rare complication” of a disease that frankly is probably going to surpass Lyme disease in sheer numbers and devastation.  Few are studying Bartonella and fewer yet are connecting it to Lyme/MSIDS, yet so many of us have it.

I saw bold, colored pictures of Bartonella in skin, bone, brain, liver, heart, synovial fluid, blood, and the prostrate.  In other words, everywhere.  It was clearly demonstrated that Bartonella can cause long-lasting and even lethal intra-erythrocytic (inside red blood cells) bacteremia in mammals.

In the abstract above, a toddler has a true bone infection from being chronically and inadequately treated for Bartonella.  Being only 3, this study is informative in that this type of infection doesn’t take a long period of time to occur.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884909/  This next link explains that due to facial skeletal anatomy, a bone infection here is more difficult to treat. Bones involved in osteomyelitis of the skull include the mandible, frontal bone, maxilla, nasal bone, temporal bone, and skull base bones.  (Those of you with facial pain can probably identify with this)

While they state it is rare and mostly happens in third-world countries, Bart is going to blow that myth to the wind.

https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/  This link corroborates the above link in that one of the mechanisms of Bart is to compress blood vessels, causing inflammation and edema of the area it infects.  In this case, the marrow.  This of course compromises blood flood and perpetuates a ripe area for the infection to abide.  This explains why the bottoms of our feet feel like someone beat them with a hammer.

In the talks on Bart, I learned that it was all over the area when a port was removed from a patient, indicating the need for continuing treatment to clear up the Bartonella infection in the surrounding tissue.  Please share this information with your doctor.

For more on Bartonella:

https://madisonarealymesupportgroup.com/2018/05/07/fox-news-bartonella-is-the-new-lyme-disease/

https://madisonarealymesupportgroup.com/2018/02/07/finally-rt-pcr-detected-bartonella-henselae-dna-on-tissue-valve/

https://madisonarealymesupportgroup.com/2017/09/13/dr-fox-cat-scratch-fever-warning/

https://madisonarealymesupportgroup.com/2017/05/11/bartonella-henselae-in-children-with-congenital-heart-disease/

https://madisonarealymesupportgroup.com/2017/01/04/endocarditis-consider-bartonella/

https://madisonarealymesupportgroup.com/2016/08/09/a-bartonella-story/

Category:

Bartonella, Lyme, research, Testing, Treatment

Study Shows Lyme/MSIDS Patients Infected With Many Pathogens and Explains Why We Are So Sick

**UPDATE May 2022**

This important article was retracted in Feb. 2022 due to:

The main method utilised in this study is an ELISA assay. An investigation by the University of Jyväskylä, Finland, has concluded that the patient selection and description in this Article, and in an unpublished report validating the methods used, do not justify the results presented. The Editors therefore no longer have confidence in the results and conclusions presented in this Article.

Please note that the scientists disagree with the retraction:

Kunal Garg, Leena Meriläinen, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher and Leona Gilbert disagree with this retraction. Ole Franz did not respond to correspondence from the Editors about this retraction.

I can only surmise that ‘the powers that be’ are not happy with the attention this work has gotten and therefore want to erase it from history.

https://www.nature.com/articles/s41598-018-34393-9?fbclid=IwAR3k-zPy2rJu8OuFl3HHqJ0twLPJvQrxiIUALUs0T-BuuJ50_1VQVwcflIQ (Please see comment at end of article)

Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases

Kunal Garg, Leena Meriläinen, Ole Franz, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher & Leona Gilbert
Scientific Reportsvolume 8, Article number: 15932 (2018)   https://doi.org/10.1038/s41598-018-34393-9

Abstract
There is insufficient evidence to support screening of various tick-borne diseases (TBD) related microbes alongside Borrelia in patients suffering from TBD. To evaluate the involvement of multiple microbial immune responses in patients experiencing TBD we utilized enzyme-linked immunosorbent assay. Four hundred and thirty-two human serum samples organized into seven categories followed Centers for Disease Control and Prevention two-tier Lyme disease (LD) diagnosis guidelines and Infectious Disease Society of America guidelines for post-treatment Lyme disease syndrome. All patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD. Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes. We have established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria. This study indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone.

A paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections.
Please see link for full article.  Snippets below:

Introduction
Tick-borne diseases (TBDs) have become a global public health challenge and will affect over 35% of the global population by 20501. The most common tick-borne bacteria are from the Borrelia burgdorferi sensu lato (s.l.) group. However, ticks can also transmit co-infections like Babesia spp.2, Bartonella spp.3, Brucella spp.4,5,6,7,8, Ehrlichia spp.9, Rickettsia spp.10,11, and tick-borne encephalitis virus12,13,14. In Europe and North America, 4–60% of patients with Lyme disease (LD) were co-infected with Babesia, Anaplasma, or Rickettsia11,15,16. Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

The two-tier guidelines36,37,38 for diagnosing LD by the Centers for Disease Control and Prevention (CDC) have been challenged due to the omission of co-infections and non-tick-borne opportunistic infections crucial for comprehensive diagnosis and treatment39,40. Emerging diagnostic solutions have demonstrated the usefulness of multiplex assays to test for LD and tick-borne co-infections41,42. However, these new technologies do not address seroprevalence of non-tick-borne opportunistic infections in patients suffering from TBD and they are limited to certain co-infections41,42. Non-tick-borne opportunistic microbes can manifest an array of symptoms24,29 concerning the heart, kidney, musculoskeletal, and the central nervous system as seen in patients with Lyme related carditis43, nephritis44, arthritis45, and neuropathy46, respectively. Therefore, Chlamydia spp., Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Human parvovirus B19, Mycoplasma spp., and other non-tick-borne opportunistic microbes play an important role in the differential diagnosis of LD24,29. As the current knowledge regarding non-tick-borne opportunistic microbes is limited to their use in differential diagnosis of LD, it is unclear if LD patients can present both tick-borne co-infections and non-tick-borne opportunistic infections simultaneously.

For the first time, we evaluate the involvement of Borrelia spirochetes, Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic microbes together in patients suffering from different stages of TBD. To highlight the need for multiplex TBD assays in clinical laboratories, we utilized the Bradford Hill’s causal inference criteria47 to elucidate the likelihood and plausibility of TBD patients responding to multiple microbes rather than one microbe. The goal of this study is to advocate screening for various TBD microbes including non-tick-borne opportunistic microbes to decrease the rate of misdiagnosed or undiagnosed48 cases thereby increasing the health-related quality of life for the patients39, and ultimately influencing new treatment protocol for TBDs.

Results
Positive IgM and IgG responses by CDC defined acute, CDC late, CDC negative, PTLDS immunocompromised, and unspecific patients to 20 microbes associated with TBD (Fig. 1) were utilized to evaluate polymicrobial infections (Figs 2–4). Patient categories included CDC acute (n = 43), CDC late (n = 43), CDC negative (n = 46), PTLDS (n = 31), immunocompromised (n = 61), unspecific (n = 31), and healthy (n = 177).

Polymicrobial infections are present at all stages of tick-borne diseases.

Microbes include Borrelia burgdorferi sensu stricto, Borrelia afzelii, Borrelia garinii, Borrelia burgdorferi sensu stricto persistent form, Borrelia afzelii persistent form, Borrelia garinii persistent form, Babesia microti, Bartonella henselae, Brucella abortus, Ehrlichia chaffeensis, Rickettsia akari, Tick-borne encephalitis virus (TBEV), Chlamydia pneumoniae, Chlamydia trachomatis, Coxsackievirus A16 (CVA16), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Mycoplasma pneumoniae, Mycoplasma fermentans, and Human parvovirus B19 (HB19V).

In Fig. 2A, 51% and 65% of patients had IgM and IgG responses to more than one microbe, whereas 9% and 16% of patients had IgM and IgG responses to only one microbe, respectively. Immune responses to Borrelia persistent forms (all three species) for IgM and IgG were 5–10% higher compared to Borrelia spirochetes in all three species (Fig. 2B). Interestingly, the probability that a randomly selected patient will respond to Borrelia persistent forms rather than the Borrelia spirochetes (Fig. S2) is 80% (d = 1.2) for IgM and 68% for IgG (d = 0.7). Figure 2A and B indicated that IgM and IgG responses by patients from different stages of TBDs are not limited to only Borrelia spirochetes.

In Fig. 3 sub-inlets, more than 50% of the patients reacted to only the individual Borrelia strains suggesting that Borrelia antigens are not cross-reactive. If patients were cross-reacting among antigens, a larger percentage of the patients would be seen with the combination of all three species (Fig. S2). These results provide evidence to suggest that the inclusion of different Borrelia species and their morphologies in current LD diagnostic tools will improve its efficiency.

Discussions
The study outcome indicated that polymicrobial infections existed at all stages of TBD with IgM and IgG responses to several microbes (Fig. 2). Results presented in this study propose that infections in patients suffering from TBDs do not obey the one microbe one disease Germ Theory. Based on these results and substantial literature11,15,16,17,27,49,50,51 on polymicrobial infections in TBD patients, we examined the probability of a causal relationship between TBD patients and polymicrobial infections following Hill’s nine criteria47.

An average effect size of d = 1.5 for IgM and IgG (Fig. 4A) responses is considered very large52. According to common language effect size statistics53, d = 1.5 indicates 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to only Borrelia. Reports from countries such as Australia27, Germany49, Netherlands11, Sweden50, the United Kingdom51, the USA15,16, and others indicate that 4% to 60% of patients suffer from LD and other microbes such as Babesia microti and human granulocytic anaplasmosis (HGA). However, previous findings11,15,16,27,49,50,51 are limited to co-infections (i.e., Babesia, Bartonella, Ehrlichia, or Rickettsia species) in patients experiencing a particular stage of LD (such as Erythema migrans). In contrast, a broader spectrum of persistent, co-infections, and opportunistic infections associated with diverse stages of TBD patients have been demonstrated in this study (Fig. 2). From a clinical standpoint, the likelihood for IgM and IgG immune responses by TBD patients to the Borrelia spirochetes versus the Borrelia persistent forms, and responses to just Borrelia versus Borrelia with many other TBD microbes has been quantified for the first time (Fig. S2).

Borrelia pathogenesis could predispose individuals to polymicrobial infections because it can suppress, subvert, or modulate the host’s immune system18,19,20,21,22 to create a niche for colonization by other microbes54. Evidence in animals55 and humans11,15,16,27,49,50,51 frequently indicate co-existence of Borrelia with other TBD associated infections. Interestingly, IgM and IgG immune levels by patients to multiple forms of Borrelia resulted in immune responses to 14 other TBD microbes (Fig. 4B). In contrast, patient responses to either form of Borrelia (spirochetes or persistent forms) resulted in reactions to an average of 8 other TBD microbes (Fig. 4B). Reaction to two forms of Borrelia reflected an increase in disease severity indicating biological gradient for causation as required by Hill’s criteria47.

Multiple microbial infections in TBD patients seem plausible because ticks can carry more than eight different microbes depending on tick species and geography56,57. Moreover, Qiu and colleagues reported the presence of at least 18 bacterial genera shared among three different tick species and up to 127 bacterial genera in Ixodes persulcatus58. Interestingly, research indicates Chlamydia-like organism in Ixodes ricinus ticks and human skin59 that may explain immune responses to Chlamydia spp., seen in this study (Fig. 2). Additionally, prevalence of TBD associated co-infections such as B. abortus, E. chaffeensis, and opportunistic microbes such as C. pneumoniae, C. trachomatis, Cytomegalovirus, Epstein-Barr virus, and M. pneumoniae have been recorded in the general population of Europe and the USA (Table S2). However, true incidence of these microbes is likely to be higher considering underreporting due to asymptomatic infections and differences in diagnostic practices and surveillance systems across Europe and in the USA. More importantly, clinical evidence for multiple microbes has been reported in humans11,15,16,27,49,50,51, and livestock55 to mention the least. Our findings regarding the presence of polymicrobial infections at all stages of TBD further supports the causal relationship between TBD patients and polymicrobial infections (Fig. 2). Various microbial infections in TBD patients have been linked to the reduced health-related quality of life (HRQoL) and increased disease severity39.

An association between multiple infections and TBD patients relates well to other diseases such as periodontal, and respiratory tract diseases. Oral cavities may contain viruses and 500 different bacterial species60. Our findings demonstrate that TBD patients may suffer from multiple bacterial and viral infections (Fig. 4). In respiratory tract diseases, influenza virus can stimulate immunosuppression and predispose patients to bacterial infections causing an increase in disease severity61. Likewise, Borrelia can induce immunosuppression that may predispose patients to other microbial infections causing an increase in disease severity.

Traditionally, positive IgM immune reaction implies an acute infection, and IgG response portrays a dissemination, persistent or memory immunity due to past infections. Depending on when TBD patients seek medical advice, the level of anti-Borrelia antibodies can greatly vary as an Erythema migrans (EM) develops and may present with IgM, IgG, collective IgM/IgG, or IgA62. This study recommends both IgM and IgG in diagnosing TBD (Figs 5 and S4–S6) as unconventional antibody profiles have been portrayed in TBD patients. Presence of long-term IgM and IgG antibodies have been reported in LD patients that were tested by the CDC two-tier system. In 2001, Kalish and colleagues reported anti-Borrelia IgM or IgG persistence in patients that suffered from LD 10–20 years ago63. Similarly, Hilton and co-workers recorded persistent anti-Borrelia IgM response in 97% of late LD patients that were considered cured following an antibiotic treatment64.

Similar events of persistent IgM and IgG antibody reactions were demonstrated in patients treated for Borrelia arthritis and acrodermatitis chronica atrophicans65, chronic cutaneous borreliosis66, and Lyme neuroborreliosis67. A clear phenomenon of immune dysfunction is occurring, which might account for the disparities in LD patient’s antibody profiles and persistence. Borrelia suppresses the immune system by inhibition of antigen-induced lymphocyte proliferation18, reducing Langerhans cells by downregulation of major histocompatibility complex class II molecules on these cells19, stimulating the production of interleukin-10 and anti-inflammatory immunosuppressive cytokine20, and causing disparity in regulation and secretion of cytokines21. Other studies have demonstrated low production or subversion of specific anti-Borrelia antibodies in patients with immune deficiency status22.

In the USA alone, the economic healthcare burden for patients suffering from LD and ongoing symptoms is estimated to be $1.3 billion per year69. Additionally, 83% of all TBD diagnostic tests performed by the commercial laboratories in the USA accounted for only LD70. Globally, the commercial laboratories’ ability to diagnose LD has increased by merely 4% (weighted mean for ELISA sensitivity 62.3%) in the last 20 years71. This study provides evidence regarding polymicrobial infections in patients suffering from different stages of TBDs. Literature analyses and results from this study followed Hill’s criteria indicating a causal association between TBD patients and polymicrobial infections. Also, the study outcomes indicate that patients may not adhere to traditional IgM and IgG responses.

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**Comment**

For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m thankful they included Bartonella as that one is often omitted but definitely a player.  I’m also thankful for the mention of viruses as they too are in the mix.  The mention of the persister form must be recognized as well as many out there deny its existence.

Key Quote:  “Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

But there is another important point.

According to this review, 83% of all commercial tests focus only on Lyme (borrelia), despite the fact we are infected with more than one microbe.  The review also states it takes 11 different visits to 11 different doctors, utilizing 11 different tests to be properly diagnosed.  https://www.news-medical.net/news/20181101/Tick-borne-disease-is-multiple-microbial-in-nature.aspx?

This is huge.  Please spread the word.

Category:

Babesia, Bartonella, Borrelia Miyamotoi (Relapsing Fever Group), Ehrlichiosis, Heart Issues, Inflammation, Lyme, Parasites, research, Rickettsia, Rocky Mountain Spotted Fever, Testing, Tickborne Relapsing Fever, Ticks, Viruses

Tick, Flea, & Louse-Borne Diseases of Public Health & Veterinary Significance in Nigeria

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6136614/

Tick, Flea, and Louse-Borne Diseases of Public Health and Veterinary Significance in Nigeria

Oluwaseun Oguntomole, Ugochukwu Nwaeze, and Marina E. Eremeeva*

Abstract

Mosquito-borne diseases are common high-impact diseases in tropical and subtropical areas. However, other non-mosquito vector-borne pathogens (VBPs) may share their geographic distribution, seasonality, and clinical manifestations, thereby contributing their share to the morbidity and mortality caused by febrile illnesses in these regions. The purpose of this work was to collect and review existing information and identify knowledge gaps about tick, flea-, and louse-borne diseases of veterinary and public health significance in Nigeria. Full-length articles about VBPs were reviewed and relevant information about the vectors, their hosts, geographic distribution, seasonality, and association(s) with human or veterinary diseases was extracted. Specific laboratory tools used for detection and identification of VBPs in Nigeria were also identified. A total of 62 original publications were examined. Substantial information about the prevalence and impacts of ticks and fleas on pet and service dogs (18 articles), and livestock animals (23 articles) were available; however, information about their association with and potential for causing human illnesses was largely absent despite the zoonotic nature of many of these peri-domestic veterinary diseases.

Recent publications that employed molecular methods of detection demonstrated the occurrence of several classic (Ehrlichia canis, Rickettsia africae, Bartonella sp.) and emerging human pathogens (R. aeschlimannii, Neoehrlichia mikurensis) in ticks and fleas. However, information about other pathogens often found in association with ticks (R. conorii) and fleas (R. typhi, R. felis) across the African continent was lacking. Records of louse-borne epidemic typhus in Nigeria date to 1947; however, its current status is not known. This review provides an essential baseline summary of the current knowledge in Nigeria of non-mosquito VBPs, and should stimulate improvements in the surveillance of the veterinary and human diseases they cause in Nigeria. Due to increasing recognition of these diseases in other African countries, veterinary and public health professionals in Nigeria should expand the list of possible diseases considered in patients presenting with fever of unknown etiology.

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**Comment**

I find it increasingly interesting that everyone’s picking up Bartonella, yet it’s hardly on the radar here despite thousands of Lyme/MSIDS patients having symptoms of it.  Bartonella is a tough pathogen & can be the guy behind so many psychiatric issues as well as heart issues.

We need to know for certain ticks can transmit it because if they don’t, either the tick bite itself is reactivating a latent infection or we are coming by it another way.  One thing’s for certain:  it needs to be dealt with on the research front as well as on the medical front.

For more on Bartonella:  https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/

https://madisonarealymesupportgroup.com/2018/10/02/1st-documented-case-of-girl-with-blood-stream-infection-with-bartonella-with-coinfection-of-another-bartonella-strain/

https://madisonarealymesupportgroup.com/2018/10/02/bartonella-found-in-deer-flies-deer-moose/

https://madisonarealymesupportgroup.com/2018/09/28/bartonella-infective-endocarditis-with-dissemination-a-case-report-literature-review/

https://madisonarealymesupportgroup.com/2016/08/09/a-bartonella-story/

For a great read on how those working with animals are especially vulnerable to Bartonella:  https://madisonarealymesupportgroup.com/2018/09/20/humana-bartonellosis-perspectives-of-a-veterinary-internist/

Excerpt:

 

Due to extensive contact with a spectrum of animal species, veterinary professionals appear to have an occupational risk of infection because of frequent exposure to Bartonella spp., therefore these individuals should exercise increased precautions to avoid arthropod bites, arthropod feces (i.e. fleas and lice), animal bites or scratches and direct contact with bodily fluids from sick animals. As Bartonella spp. have been isolated from cat, dog or human blood, cerebrospinal fluid, joint fluid,aqueous fluid, seroma fluid and from pleural, pericardial and abdominal effusions, a substantial number of diagnostic biological samples collected on a daily basis in veterinary practices could contain viable bacteria.
The increasing number of defined Bartonella spp., in conjunction with the high level of bacteremia found in reservoir adapted hosts, which represent the veterinary patient population, ensures that all veterinary professionals will experience frequent and repeated exposure to animals harboring these bacteria. Therefore, personal protective equipment, frequent hand washing and avoiding cuts and needle sticks have become more important as our knowledge of this genus has improved and various modes of transmission have been defined.
Physicians should be educated as to the large number of Bartonella spp. in nature, the extensive spectrum of animal reservoir hosts, the diversity of confirmed and potential arthropod vectors, current limitations associated with diagnosis and treatment efficacy, and the ecological and evolving medical complexity of these highly evolved intravascular, endotheliotropic bacteria.

Category:

Bartonella, Ehrlichiosis, mosquitoes, research, Rickettsia, Testing, Ticks