Linda’s comments:  Yeaaaa for the Vets….I support them 100%…we expect them to fight for our lives and freedom then make them sick and refuse to acknowledge the problems….I hope they win…

Full article: http://www.aolnews.com/nation/article/sick-vets-sue-government-contractor-kbr-over-trash-fires-in-iraq-afghanistan/19583671?icid=main|htmlws-main-n|dl1|link4|http%3A%2F%2Fwww.aolnews.com%2Fnation%2Farticle%2Fsick-vets-sue-government-contractor-kbr-over-trash-fires-in-iraq-afghanistan%2F19583671

Excerpt:

(Aug. 6) — Hundreds of Americans who got sick after working in Iraq and Afghanistan are suing government contractor KBR, claiming they were poisoned by toxic smoke from trash fires on U.S. military bases there, The Washington Post reports today.

According to a lawsuit filed in federal court in Maryland, 241 service veterans and contractors are suing the Houston-based firm, which was in charge of burning trash — including Styrofoam, plastic, solvents, medical waste and even dead animals — at several American bases before the military limited so-called burn pits earlier this year.

Joe Raedle, An Afghan man looks through garbage as some of it burns at a dump at the Bagram air base in Afghanistan in 2002. Americans who worked in Afghanistan and Iraq say exposure to such fires has led to breathing disorders and cancers.

Full article: http://www.medicalnewstoday.com/articles/196744.php

Excerpt:

A possible cause of irritable bowel syndrome has been traced to a small piece of RNA that blocks a substance protecting the colon membrane, leading to hostile conditions that can produce diarrhea, bloating and chronic abdominal pain.

New research shows that this RNA segment sends signals that stop the activity of the gene that produces glutamine, an amino acid. Previous research has linked a shortage of glutamine in the gut with the seepage of toxins and bacteria through the intestinal wall, irritating nerves and creating disease symptoms.

Scientists say that trying to generate glutamine in the disordered bowel by silencing this RNA segment could open up a whole new way of thinking about treating the diarrhea-predominant type of irritable bowel syndrome (IBS). In the meantime, they are making plans to conduct a clinical trial to see if glutamine supplements could also reduce common IBS symptoms

This form of the disorder is characterized by diarrhea and bloating as well as chronic abdominal pain that is difficult to treat. About a third of IBS patients have the diarrhea-predominant type, another third experience consistent constipation, and the rest experience alternating bouts of diarrhea and constipation.

Full article: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20666055&retmode=ref&cmd=prlinks

Excerpt:

Lyme disease is a multisystem infectious disease, endemic in
parts of Europe, including the West of Ireland. Neurological
manifestions (neuroborreliosis) are variable. Presenting
neurological syndromes include meningitis, cranial neuropathies,
myeloradiculitis and mononeuritis multiplex. A lack of
specificity in serological diagnosis may add to diagnostic
confusion. We reviewed thirty cases of acute Lyme disease in the
West of Ireland and found neurological syndromes in 15 (50%),
with painful radiculopathy (12 patients; 80%) and cranial
neuropathy (7 patients; 46%) occurring frequently.
Neuroborreliosis needs to be considered in the differential
diagnosis of these neurological syndromes in the appropriate
clinical context.

Full article: http://jnnp.bmj.com/content/78/12/1409.extract

Excerpt:

Retrobulbar optic neuritis (RON) is an unusual complication of Lyme disease. The diagnosis of early Lyme disease is difficult, and the relationship between RON and Lyme disease remains controversial. None of the 14 cases of optic neuritis described in the literature in association with Lyme disease fulfilled the Halperin and Sibony criteria for active Lyme disease. We report the first case of acute Lyme disease complicated by RON established using the Halperin and Sibony criteria.

Lyme disease is a multisystem infectious disease caused by tick borne spirochetes of the Borrelia burgdorferi group. Diagnosis of this infection can be difficult and serological testing such as western blot can be useful. Cranial neuropathies are common but RON has been reported in a few isolated cases.1 A causal link between optic neuritis and Lyme disease has not been established and remains controversial. We report a case of active neuro-Lyme disease complicated by RON

Full article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904298/?tool=pubmed

Excerpt:

Several pathogenic Rickettsia species can be transmitted via Ixodes ricinus ticks to humans and animals. Surveys of I. ricinus for the presence of Rickettsiae using part of its 16S rRNA gene yield a plethora of new and different Rickettsia sequences. Interpreting these data is sometimes difficult and presenting these findings as new or potentially pathogenic Rickettsiae should be done with caution: a recent report suggested presence of a known human pathogen, R. australis, in questing I. ricinus ticks in Europe. A refined analysis of these results revealed that R. helvetica was most likely to be misinterpreted as R. australis. Evidence in the literature is accumulating that rickettsial DNA sequences found in tick lysates can also be derived from other sources than viable, pathogenic Rickettsiae. For example, from endosymbionts, environmental contamination or even horizontal gene transfer.

Full article: http://www.amc.edu/amr/archives/200606/case1.html

Excerpt:

A 52-year-old male marathon runner with a past medical history significant for glaucoma presented to the emergency department with a two-week history of increasing fatigue after an episode of syncope.

He initially presented to his primary care doctor’s office complaining of flu like symptoms one week after running a marathon and three weeks prior to admission. He described fever, chills, night sweats, increasing fatigue and body aches. He was noted to be an avid runner who had finished within the top five to ten athletes in prior marathons. He stated that despite training intensely, he only finished in 50th place. During this visit, a chest x-ray was obtained which showed no evidence of pneumonia or other abnormalities. He was diagnosed with a minor viral upper respiratory tract infection and over the following week began to notice improvement of his symptoms.

He returned to the office two weeks after the initial visit with worsening fatigue and decreased exercise tolerance. He had become increasingly short of breath after running more than 2 milles. A serologic test for Lyme disease was performed to rule out Lyme carditis after an EKG showed first-degree heart block.

Excerpt:

Human monocytotropic ehrlichiosis is caused by Ehrlichia chaffeensis, a Gram-negative bacterium lacking lipopolysaccharide. We have shown that fatal murine ehrlichiosis is associated with CD8(+)T cell-mediated tissue damage, tumor necrosis factor-alpha, and interleukin (IL)-10 overproduction, and CD4(+)Th1 hyporesponsiveness. In this study, we examined the relative contributions of natural killer (NK) and NKT cells in Ehrlichia-induced toxic shock. Lethal ehrlichial infection in wild-type mice induced a decline in NKT cell numbers, and late expansion and migration of activated NK cells to the liver, a main infection site that coincided with development of hepatic injury. The spatial and temporal changes in NK and NKT cells in lethally infected mice correlated with higher NK cell cytotoxic activity, higher expression of cytotoxic molecules such as granzyme B, higher production of interferon-gamma and tumor necrosis factor-alpha, increased hepatic infiltration with CD8alphaCD11c(+) dendritic cells and CD8(+)T cells, decreased splenic CD4(+)T cells, increased serum concentrations of IL-12p40, IL-18, RANTES, and monocyte chemotactic protein-1, and elevated production of IL-18 by liver mononuclear cells compared with nonlethally infected mice. Depletion of NK cells prevented development of severe liver injury, decreased serum levels of interferon-gamma, tumor necrosis factor-alpha, and IL-10, and enhanced bacterial elimination. These data indicate that NK cells promote immunopathology and defective anti-ehrlichial immunity, possibly via decreasing the protective immune response mediated by interferon-gamma producing CD4(+)Th1 and NKT cells.

Full article: http://onlinelibrary.wiley.com/doi/10.1111/j.1939-1676.2010.0563.x/abstract

Excerpt:

Suspected Needle Stick Transmission of Bartonella vinsonii

subspecies berkhoffii to a Veterinarian

1. A.M. Oliveira¹,
2. R.G. Maggi¹,
3. C.W. Woods²,
4. E.B. Breitschwerdt¹

Article first published online: 2 AUG 2010

DOI: 10.1111/j.1939-1676.2010.0563.x

Full article: http://sci.tech-archive.net/Archive/sci.med.diseases.lyme/2008-06/msg00078.html

Excerpt:

IDSA knows that chronic Lyme exists

The IDSA is aware that chronic Lyme exists. We know this because
members of the 2000 and 2006 Lyme disease guideline panels wrote, in
research articles and patents, that chronic Lyme exists.

Evidence about the existence of chronic Lyme borreliosis has increased
since the 2006 LD guidelines were published.

Scientists in California recently reported that not only can Bb persist
in mice despite treatment with ceftriaxone, but the Borrelia can also
infect other ticks and mice. (1) This study buttresses previous
studies that showed that Borrelia can persist in mice (2, 3), dogs (4,
5, 6), and ponies (7).

Studies have also shown that Bb can persist despite antibiotic
treatment in the following human cells, tissues, organs, and body
fluids:

* Fibroblasts (8; Mark Klempner, an IDSA LD guideline panel member in
2006, is an author of this study)

Full article: http://www.miklossy.ch/452/index.html

Excerpt:

Treponema pallidum and Borrelia burgdorferi spirochetes, in late syphilis and late Lyme disease can cause cerebral infarct and cognitive decline (dementia) in parenchymatous neurosyphilis and Lyme neuroborreliosis.

The cognitive decline (dementia)  is caused by the direct invasion of brain parenchyma by spirochetes (direct parenchymal involvement) years or decades follwoing the primary infection.

Cerebral infarcts in the meningovascular form of neurospirochetoses (Meningovascular form of neurosyphilis and Lyme neuroborreliosis) is not caused by spirochetal invasion of brain tissue. The parenchymal involvement is secondary to the occlusion of the affected meningeal arteries. It may lead to”vascular” dementia.