Archive for the ‘research’ Category

Rickettsia Found in Ticks on Brazilian Snakes

https://www.ncbi.nlm.nih.gov/m/pubmed/30484879/

Microorganisms in the ticks Amblyomma dissimile Koch 1844 and Amblyomma rotundatum Koch 1844 collected from snakes in Brazil.

Ogrzewalska M, et al. Med Vet Entomol. 2018.

Abstract

Knowledge about ticks (Acari) and screening of ticks parasitizing various hosts are necessary to understand the epidemiology of tick-borne pathogens. The objective of this study was to investigate tick infestations on snakes (Reptilia: Squamata: Serpentes) arriving at the serpentarium at the Institute Vital Brazil, Rio de Janeiro. Some of the identified ticks were individually tested for the presence of bacteria of the genera Rickettsia (Rickettsiales: Rickettsiaceae), Borrelia (Spirochaetales: Spirochaetaceae), Coxiella (Legionellales: Coxiellaceae), Bartonella (Rhizobiales: Bartonellaceae), Ehrlichia (Rickettsiales: Anaplasmataceae), Anaplasma (Rickettsiales: Anaplasmataceae), and Apicomplexa protozoa of the genera Babesia (Piroplasmida: Babesiidae) and Hepatozoon (Eucoccidiorida: Hepatozoidae).

A total of 115 hard ticks (Ixodida: Ixodidae) were collected from 17 host individuals obtained from four Brazilian states. Two species of tick were identified: Amblyomma dissimile Koch 1844 (four larvae, 16 nymphs, 40 adults), and Amblyomma rotundatum Koch 1844 (12 nymphs, 43 adults).

Rickettsia bellii was found in A. rotundatum and A. dissimile ticks and Rickettsia sp. strain Colombianensi, Anaplasma-like and Hepatozoon sp. in A. dissimile ticks. Among the tested ticks, no DNA of Borrelia, Bartonella, Coxiella or Babesia was found. The present findings extend the geographic range of Rickettsia sp. strain Colombianensi in Brazil and provide novel tick-host associations.

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**Comment**

Great example of how we need to expand our minds regarding ticks and the hosts they feed on.  For far too long the white footed mouse has been the sole perp blamed along with the black-legged tick.  There are many other ticks transmitting disease and many other hosts.

Please understand that researchers in their vying for dollars want to simplify and whittle things down into a narrow, confined project.  Unfortunately, nothing about Lyme/MSIDS is simple or narrow and this type of thinking has hurt patients for over 40 years.

More is coming out on the importance of birds transiting ticks everywhere:  https://madisonarealymesupportgroup.com/2018/11/07/ticks-on-the-move-due-to-migrating-birds-and-photoperiod-not-climate-change/

https://madisonarealymesupportgroup.com/2018/06/08/hemorrhagic-fever-virus-found-on-ticks-on-migratory-birds/

Key quote:

“We see that infectious diseases can spread to new geographical areas and that is why it is necessary to understand the role of different animal species in the dynamics of these diseases,” says Tove Hoffman.

https://madisonarealymesupportgroup.com/2018/11/05/hawk-found-carrying-asian-long-horned-tick-the-one-that-drains-cattle-of-all-their-blood/

https://madisonarealymesupportgroup.com/2017/08/17/of-birds-and-ticks/

Lizards must be factored in as well:  https://madisonarealymesupportgroup.com/2018/06/25/the-confounding-geography-of-lyme-disease-in-the-u-s/

And for Wisconsinites, lizards are a problem here too:

Researchers working at Fort McCoy near Sparta, as part of a multi-university project Michigan State ecologist Jean Tsao leads, have collected deer ticks from five-lined skinks and snakes.

For pictures and the geographical range of WI skinks, see (yes, they are in Dane County):  https://dnr.wi.gov/topic/WildlifeHabitat/Herps.asp?mode=detail&spec=ARACH01050

Category:

Anaplasmosis, Lyme, research, Rickettsia, Testing, Ticks

IPAK Model of Autism Spectrum Causality

http://ipaknowledge.org/ASD-Causality-Model.php

“Personal Communication, Dr. J. Lyons-Weiler, The Institute for Pure and Applied Knowledge”

The IPAK Model of ASD Causality (aka “The IPAK Model”)

After reviewing thousands of studies over two years, a more complete picture of the causality of ASD has now emerged.

We are working on an interactive web resource to allow the public and researchers to access the scientific literature in support of each component of this ASD causality model.

Note that this model includes an important component of genetic susceptibility, never addressed in whole-population ecological correlational association studies.

Again, the hypothesis of genetic susceptibility has not been addressed.

USAGE: Please use with citation and reference

Also available for download as .tiff, .ppt

Vaccine Metals and ER Stress

Aremu DA, Ezomo OF, Meshitsuka S. Gene expression in primary cultured astrocytes affected by aluminum: alteration of chaperons involved in protein folding. Environ Health Prev Med. 2011;16:16-24.

Franchi L, Núñez G. The Nlrp3 inflammasome is critical for aluminium hydroxide-mediated IL-1beta secretion but dispensable for adjuvant activity. Eur J Immunol. 38(8):2085-9.

Rizvi SH, Parveen A, Ahmad I, Ahmad I, Verma AK, Arshad M, Mahdi AA. Aluminum Activates PERK-EIF2α Signaling and Inflammatory Proteins in Human Neuroblastoma SH-SY5Y Cells. Biol Trace Elem Res. 2016;172(1):108-19.

Rizvi MSH, Parveen A, Verma AK, Ahmad I, Arshad M, Mahdi AA. Aluminium induced endoplasmic reticulum stress mediated cell death in SH-SY5Y neuroblastoma cell line is independent of p53. PLoS One. 2014;30;9(5):e98409.

Stamogiannos A, Papakyriakou A, Mauvais FX, van Endert P, Stratikos E. Screening Identifies Thimerosal as a Selective Inhibitor of Endoplasmic Reticulum Aminopeptidase 1. ACS Med Chem Lett. 2016;7:681-5.

Direct Mitotoxicity

Kahrizi F 2016. Repeated Administration of Mercury Intensifies Brain Damage in Multiple Sclerosis through Mitochondrial Dysfunction. Iran J Pharm Res. 15:834-841.

Lemire et al., 2009. Aluminum-induced defective mitochondrial metabolism perturbs cytoskeletal dynamics in human astrocytoma cells. J. Neurosci Res 87:1474-83

Sharpe, MA et al., 2012. Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA Journal of Toxicology Volume 2012 Article ID 373678, 12 pages.

Vaccine ER Stress + Unfolded Protein ER Stress = ER Hyperstress

Lyons-Weiler, J. 2018. Autism is an Acquired Cellular Detoxification Deficiency Syndrome with Hetergeneous Genetic Predisposition. Autism Open Access, (Publisher’s “editing version” online: https://www.omicsonline.org/open-access/autism-is-an-acquired-cellular-detoxification-deficiency-syndrome-with-heterogeneous-genetic-predisposition-2165-7890-1000224.pdf

ER Hyperstress -> Impaired Cellular Detoxification

ER/Mito/Golgi Citations in: Lyons-Weiler, J. 2018. Autism is an Acquired Cellular Detoxification Deficiency Syndrome with Hetergeneous Genetic Predisposition. Autism Open Access, (Publisher’s “editing version” online: https://www.omicsonline.org/open-access/autism-is-an-acquired-cellular-detoxification-deficiency-syndrome-with-heterogeneous-genetic-predisposition-2165-7890-1000224.pdf

Leaky Gut -> Absorption of Toxins

De Chambrun G.P., Body-Malapel M., Frey-Wagner I., Djouina M., Deknuydt F., Atrott K., Vignal C. Aluminum enhances inflammation and decreases mucosal healing in experimental colitis in mice. Mucosal Immunol. 2014;7:589–601.

Kirschbaum, BB and C Schoolwerth. 1989. Acute Aluminum Toxicity Associated with Oral Citrate and Aluminum-Containing Antacids. The American Journal of the Medical Science 297:9-11.

Tian F. 2017. The therapeutic protection of a living and dead Lactobacillus strain against aluminum-induced brain and liver injuries in C57BL/6 mice. PLoS One. 12:e0175398. doi: 10.1371/journal.pone.0175398

Yu L 2016. Potential of Lactobacillus plantarum CCFM639 in Protecting against Aluminum Toxicity Mediated by Intestinal Barrier Function and Oxidative Stress. Nutrients. 8:pii: E783.

Yu, L 2017. Lactobacillus plantarum CCFM639 can prevent aluminium-induced neural injuries and abnormal behaviour in mice. Journal of Functional Foods 30:142-150.

Yu, L. 2017. Dietary Lactobacillus plantarum supplementation enhances growth performance and alleviates aluminum toxicity in tilapia Ecotoxicology and Environmental Safety 143:307-314.

Chronic Microglial Activation -> Leaky Gut

Grubišić V and Parpura V. 2015. The second brain in autism spectrum disorder: could connexin 43 expressed in enteric glial cells play a role? Front Cell Neurosci. 9:242. doi: 10.3389/fncel.2015.00242.

Kirchgessner AL et al., 1997. Excitotoxicity in the enteric nervous system. J Neurosci. 17(22):8804-16.

Unfolded Proteins -> Autoimmunity

Garaud JC, Schickel JN, Blaison G et al. B cell signature during inactive systemic lupus is heterogeneous: toward a biological dissection of lupus. PLoS One 2011;6:e23900.

Clavarino G, Adriouach S, Quesada JL, Clay M et al. Unfolded protein response gene GADD34 is overexpressed in rheumatoid arthritis and related to the presence of circulating anti-citrullinated protein antibodies. 2016;49(3):172-8.

Immunoneuroexcitotoxicity -> Aberrant Pruning

Cunningham CL et al., 2013. Microglia regulate the number of neural precursor cells in the developing cerebral cortex. J Neurosci. 33(10):4216-33. doi: 10.1523/JNEUROSCI.3441-12.2013. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711552/

Fiorentino et al., 2016. Blood–brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders. Molecular Autism 4:49

Strunecka A., et al. 2018. Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum. Surg Neurol Int. 2018; 9:74.

Aberrant Pruning -> Altered Development

Thomas MS. The over-pruning hypothesis of autism. Dev Sci. 2016 19(2):284-305.

Kim HJ et al. Deficient autophagy in microglia impairs synaptic pruning and causes social behavioral defects. Mol Psychiatry. 2017 22(11):1576-1584.

Vaccine Metals Release -> Autoimmunity

Tomljenovic L, Shaw CA Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations. Lupus. 2012 21(2):223-30.

Autoimmunity -> Altered Development

Braunschweig D et al., 2008. Autism: maternally derived antibodies specific for fetal brain proteins. Neurotoxicology. 29(2):226-31.

Cabanlit M et al., 2007. Brain-specific autoantibodies in the plasma of subjects with autistic spectrum disorder. Ann N Y Acad Sci. 1107:92-103.

Malkki H. Neurodevelopmental disorders: Maternal antibodies induce autism-like phenotype in mice. Nat Rev Neurol. 2016 12:678-679. doi: 10.1038/nrneurol.2016.165.

 

Category:

Activism, Autism, research, vaccines

Relapsing Fever Found at Popular Recreation Site in CA Ticks

https://www.ncbi.nlm.nih.gov/pubmed/30517684

2018 Dec 4. doi: 10.1093/jme/tjy213. [Epub ahead of print]

Borrelia parkeri in Ornithodoros parkeri (Ixodida: Argasidae) Collected Using Compact Dry Ice Traps in Madera County, California.

Osborne CJ1, Crosbie PR1, Van Laar TA1.

Abstract

Tick-borne relapsing fever (TBRF) is a potentially serious vector-borne disease endemic to the western United States. Vector surveillance is compromised by the nidicolous life history of the three Ornithodoros species that transmit TBRF to people in this region. Large-scale stationary trapping methods were developed to survey a wide geographical range of Ornithodoros spp. which are known to vector relapsing fever Borrelia spp. in California. Ninety-six Ornithodoros parkeri were collected from four locations in the foothills of Fresno and Madera Counties. Two of these O. parkeri nymphs were PCR positive for Borrelia parkeri, and their collection at a popular recreation site increases the public health concern.

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More on Relapsing Fever:  https://igenex.com/ticktalk/2018/01/11/borreliosis-relapsing-fever-disease/

Category:

Borrelia Miyamotoi (Relapsing Fever Group), research, Ticks

Transverse Myelitis & Guillain-Barre Associated with Bartonella

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6106413/

Transverse Myelitis and Guillain-Barré Syndrome Associated with Cat-Scratch Disease, Texas, USA, 2011

Emerg Infect Dis. 2018 Sep; 24(9): 1754–1755.

Ramia Zakhour,corresponding author Pedro Mancias, Gloria Heresi, and Norma Pérez

Abstract

We describe a case of coexisting transverse myelitis and Guillain-Barré syndrome (GBS) related to infection with Bartonella henselae proteobacterium and review similar serology-proven cases. B. henselae infection might be emerging as a cause of myelitis and Guillain-Barré syndrome and should be considered as an etiologic factor in patients with such clinical presentations.

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**Comment**

This case study is of a previously healthy 10 year old girl who presented with lower extremity weakness, abdominal pain, vomiting, urinary retention, lymphadenopathy, headache, neck pain, lower back pain, burning in wrists, knees, ankles, and feet, and increases sensitivity to pain in her legs.

She had evidence of myelitis, brain lesions, and peripheral nerve involvement.

They administered rifampin and doxycycline for a possible CSD (Cat Scratch Disease) diagnosis but had to discontinue rifampin due to rising liver enzyme levels.  She was then given IV immunoglobulin for possible GBS (Guillain Barre Syndrome) and showed tremendous improvement with resolution of urinary retention and decrease in pain & weakness.  Four months later she had only residual sensory deficits.

According to the study, by 1971, 40 cases of Bartonella with neurological complications occurred with 90% involving encephalitis with a few myelopathy.  Other CSD associated myelitis cases and other GBS-associated Bartonella cases have been reported.

Key quote:

Studies of the efficacy of treatments for CSD-associated neurologic manifestations are lacking, and thus, the optimal regimen and duration of therapy are unknown. However, we suggest that clinicians consider CSD early in disease courses involving neurologic complications; the possibility of GBS, myelitis, or both in the setting of possible CSD should prompt clinicians to initiate antimicrobial treatment early and consider steroid or intravenous immunoglobulin therapy to prevent progression of disease.

For Lyme/MSIDS patients with these presentations, steroids would be counter-indicated due to the immune suppression which would enhance pathogen involvement:  http://www.lymenet.de/literatur/steroids.htm

“It is interesting to note that in dogs who had Lyme disease, injections of dexamethasone, a corticosteroid, enabled Borrelia burgdorferi to be cultured from blood drawn on the following day.”

This was done by Dr. Elizabeth Burgess at the University of Wisconsin. This suggests that the steroid suppresses a mechanism for keeping the bacteria out of the circulatory system, since ordinarily it is difficult to grow the Lyme organism from the blood. Entrance of the bacteria into the bloodstream can allow seeding of other organs.

“In conclusion, the decision to use the steroids in a Lyme patient must be given considerable thought and the possible benefits must be weighed against the risks. I would not use steroids unless the patient was also on antibiotics.“

Please keep in mind the difference between catabolic (break down) steroids and anabolic (build up) steroids.

 

 

 

 

Category:

Bartonella, research, Viruses

Bartonella Presenting with Lymphadenopathy

https://www.ncbi.nlm.nih.gov/m/pubmed/30068900/

Cat-Scratch Disease in an AIDS Patient Presenting with Generalized Lymphadenopathy: An Unusual Presentation with Delayed Diagnosis.

Mantis J, et al. Am J Case Rep. 2018.

Abstract

BACKGROUND Bartonella infection is the causative organism of cat-scratch disease (CSD), which typically presents with self-limited localized lymphadenopathy. In HIV-infected patients, Bartonella infection can cause systemic illnesses with significant morbidity and mortality manifesting as bacillary angiomatosis (BA), hepatic peliosis, splenitis, bacteremic febrile illness, and other organ involvement. To the best of our knowledge, there have been no reports of HIV-infected patients presenting with generalized lymphadenopathy caused by Bartonella infection. We report an unusual case of CSD presenting with generalized lymphadenopathy in an AIDS patient with advanced immunosuppression.

CASE REPORT A 44-year-old woman with AIDS, advanced immunosuppression, and intermittent adherence to antiretroviral therapy and medical care, presented with cough and increased generalized tender lymphadenopathy. A lymph node biopsy 1 year earlier was non-diagnostic for tuberculosis, fungal infection, and lymphoproliferative disorders. She remained with generalized lymphadenopathy. A repeat biopsy with the addition of Warthin-Starry silver staining suggested the diagnosis of cat-scratch lymphadenitis. She responded well to a long course of azithromycin antibiotic therapy, with the resolution of lymphadenopathy. CONCLUSIONS Cat-scratch disease may present with prolonged generalized lymphadenopathy, an unusual presentation in HIV patients with advanced immunosuppression. Awareness of the possibility of CSD in a similar clinical scenario may prompt early recognition and management of this disease.

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**Comment**

While this case study is on an HIV-infected patient, those infected with Lyme/MSIDS can have similar presentations with systemic illness, and significant morbidity and mortality due to the immunosuppressive nature of tick borne infections (TBI’s).

Both my husband and I had Bartonella yet no lymph-node involvement.  This checklist outlines most of the most prevalent symptoms & we had many:  https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/  (Checklist within link along with other symptoms and cases)

Notice that treatment was a “long course” of antibiotics that for some reason is acceptable for an immunosuppressed HIV patient but NOT an immunosuppressed Lyme/MSIDS patient.  It’s a head scratcher for sure.

Congenital transmission is highly likely:  https://madisonarealymesupportgroup.com/2019/01/02/bartonella-in-entire-canadian-family/

 

Category:

Bartonella, research, Testing, Treatment