Excerpt:

Results

Following inoculation with B. tamiae, mice developed ulcerative skin lesions and subcutaneous masses on the lateral thorax, as well as axillary and inguinal lymphadenopathy. B. tamiae DNA was found in subcutaneous masses, lymph node, and liver of inoculated mice. Histopathological changes were observed in tissues of inoculated mice, and severity of lesions correlated with the isolate inoculated, with the most severe pathology induced by B. tamiae Th239. Mice inoculated with Th239 and Th339 demonstrated myocarditis, lymphadenitis with associated vascular necrosis, and granulomatous hepatitis and nephritis with associated hepatocellular and renal necrosis. Mice inoculated with Th307 developed a deep dermatitis and granulomas within the kidneys.

Conclusions

The three isolates of B. tamiae evaluated in this study induce disease in immunocompetent Swiss Webster mice up to 6 weeks after inoculation. The human patients from whom these isolates were obtained had clinical presentations consistent with the multi-organ pathology observed in mice in this study. This mouse model for B. tamiae induced disease not only strengthens the causal link between this pathogen and clinical illness in humans, but provides a model to further study the pathological processes induced by these bacteria.

Plasmodium vivax is responsible for a significant portion of malaria cases worldwide, especially in Asia and Latin America, where geo-helminthiasis have a high prevalence. Impact of the interaction between vivax malaria and intestinal helminthes has been poorly explored. The objective of this study was to evaluate the influence of intestinal helminthiasis on the concentration of hemoglobin in children with Plasmodium vivax malaria in rural areas in the municipality of Careiro, in the Western Brazilian Amazon.

  Lethal and toxic levels of hydrogen sulfide, benzene, and methalene chloride are floating in the air over the oil spill. There’s a very high probability that residents exposed to the air surrounding the spill will suffer a direct hit to their health status such as debilitating diseases or various birth deformities and cancer as a long-term result. But first what these people will see is flu-like symptoms, which, like in the flu, are symptoms of intolerable amounts of foreign toxins, chemicals and heavy metals in the tissues dumping into the bloodstream.
 
     Even a small amount of benzene exposure can cause temporary nervous system disorders, immune system depression and anemia. Short-term affects include skin, eye, and respiratory tract irritation, headache, stomach irritation, drowsiness and dizziness. High levels of exposure can result in a rapid heart rate, excessive bleeding, tremors, vomiting, unconsciousness and death. Benzene can cause harmful effects on bone marrow and a decrease in red blood cells leading to myelofibrosis and myelodysplastic syndrome.
 
     That’s how it starts. Chemical exposure symptoms feel like a flu. Professor I.M. Trakhtenberg of Russia gives us a big hint when he says, “Chronic mercury exposure is also a threat to our health and makes us especially vulnerable to flu infections. It has been shown that “prolongedexposure of mammals (white mice) to low mercury concentrations (0.008 – 0.02mg/m3) leads to a significant increase in the susceptibility of mice topathological influenza virus strains.” For contemporary medicine to respond in an appropriate and humane way to the oil disaster it will have to leap out of the quagmire of its present paradigm an into one that understands the ‘terrain’ of human physiology and how that terrain is being overrun by chemical toxicity and heavy metals. WE DO NOT NEED TO BE ATTACKED BY AN INFLUENZA VIRUS STRAIN TO GET THE FLU. When we are attacked with nasty chemicals we are as likely to get the flu as when we are run over by viruses, which are more potent at driving health officials mad as at causing pandemics.
 
     “Blood elements such as WBCs, RBCs, hemoglobin, and bone marrow are adversely affected. With tissue proteins there is alteration of biological properties and protein synthesis. Enzyme; hormone; and endocrine functions of pituitary, adrenal, thyroid, ovaries, and testes are altered. There are pathological effects on the heart, liver, immune system, central nervous system, lungs, kidneys, and spleen.” continues Dr. Trakhtenberg.
 
     Thiol poisons react with SH groups of proteins, which leads to lowering the activity of various enzymes containing these proteins. This produces a series of disruptionsin the functional activity of many organs and tissues and this is the mechanism and pathological pathway of poisons that run us right into the ground. A toxic storm is gathering in the Gulf of Mexico and it contains devastating chemicals that can and will poison and destroy proteins with sulfur bonds.
 
Associated Illnesses
 
     According to the U.S. Department of Veterans Affairs, between 175,000 and 210,000 – or about 25 percent – of the living veterans of the 1991 Gulf War are currently afflicted by a debilitating, chronic, multi-symptom, multi-system disease commonly known as Gulf War Illness or Gulf War Syndrome. The Environmental Illness Resource , (http://imva.us1.list-manage.com/track/click?u=25b08cc8b5ebaf472984d04d0&id=f7a015aaa4&e=a053e43583) tells us that more than 110,000 cases had been reported by 1999, according to official government sources. There is even a report relating to military personnel in Kansas developing flu-like symptoms and chemical sensitivities after handling archived documents returned from the Gulf. In the UK, veterans of the 2003 conflict began reporting symptoms identical to those reported by the first war shortly after they returned from duty.
 
     The symptoms reported by veterans include:
 
Fatigue
Persistent Headaches
Muscle Aches/Pains
Neurological Symptoms, e.g. tingling and numbness in limbs
Cognitive Dysfunction – short-term memory loss, poor concentration, inability to take in information
Mood and Sleep Disturbances – Depression, Anxiety, Insomnia
Dermatological Symptoms – Skin Rashes, Unusual Hair Loss
Respiratory Symptoms – Persistent Coughing, Bronchitis, Asthma
Chemical Sensitivities
Gastrointestinal Symptoms – Diarrhea, Constipation, Nausea, Bloating
Cardiovascular Symptoms
Menstrual Symptoms
 
     These symptoms are similar to those attributed to chronic fatigue syndrome, multiple chemical sensitivities and other environmental illnesses. This similarity hasn’t gone unnoticed, which is why many people, including healthcare professionals and researchers, are coming to the conclusion that all these illnesses share common causes and etiologies. Gulf War vets have developed ALS, or Lou Gehrig’s disease, at twice the rate of vets who did not serve in the Gulf War. Some veterans returned seemingly well, yet developed severe illnesses months or years later. The lag time between cause and effect makes understanding these illnesses more difficult.
 
     Coalition troops were constantly exposed to chemicals (and vaccines) whose use is considered safe by people and organizations that do not know a safe substance from a dangerous one. The retreating Iraqi army ignited approximately 600 oil wells in February 1991, which burned for about nine months. These fires produced massive amounts of thick smoke that sometimes drifted to ground level causing increased exposure to ground troops. When this occurred the air pollution was far greater than would be experienced in the average traffic congested western city.
 
     Questionnaires filled in by US troops indicated higher rates of eye and upper respiratory tract irritation, shortness of breath, cough, rashes, and fatigue than unexposed troops. The smoke from oil well fires contained a cocktail of chemicals, notably benzene, hydrogen sulfide and sulfur dioxide as well as quantities of particulate matter.
 
Read The Full Article
Mark Sircus Ac., OMD
Director International Medical Veritas Association
http://publications.imva.info
http://blog.imva.info
 

Objective- To describe the current understanding of the etiology,
pathogenesis, diagnosis, and treatment of feline hemotropic
mycoplasmosis (feline infectious anemia). Data Sources-
Manuscripts published on hemotropic mycoplasmosis in cats and
other animal species, based on a search of PubMed using the
search terms
‘hemoplasmas,”haemoplasmas,”hemotropic,”haemotropic,’ and
‘Haemobartonella,’
as well as references published within manuscripts accessed.
Human Data
Synthesis- Although hemotropic bacteria such as Bartonella
bacilliformis have been recognized in humans for over 100 years,
it has only been in recent years that some of these have been
identified as hemotropic mycoplasmas. Veterinary Data Synthesis-
Three species of hemotropic mycoplasmas have been documented in
cats worldwide, Mycoplasma haemofelis, ‘Candidatus Mycoplasma
turicensis,’ and ‘Candidatus Mycoplasma haemominutum.’ These
organisms were previously known as Haemobartonella felis, but are
now known to be mycoplasmas. M. haemofelis is the most pathogenic
species, and causes anemia in immunocompetent cats. Although
‘Candidatus Mycoplasma turicensis’ and ‘Candidatus Mycoplasma
haemominutum’ may be more capable of causing anemia in
immunosuppressed cats, their pathogenicity remains controversial.
Assays based on polymerase chain reaction technology are the most
sensitive and specific diagnostic tests available for these
organisms, because they remain uncultivable in the laboratory
setting. Blood smears are unreliable for diagnosis of
hemoplasmosis because of their lack of sensitivity and
specificity. Conclusions- Cats presenting to emergency/critical
care specialists with hemolytic anemia should be tested using
polymerase chain reaction assays for hemotropic mycoplasmas
before instituting antimicrobial therapy. Positive test results
for M. haemofelis suggest involvement of this organism in
hemolytic anemia. Other differential diagnoses for hemolytic
anemia should be considered in cats testing positive for
‘Candidatus Mycoplasma turicensis’ and ‘Candidatus Mycoplasma
haemominutum,’ because the presence of these organisms is not
always associated with anemia.

Excerpt:

We conducted a prospective study to determine causes of acute febrile illness in 4 community hospitals, 2 in Chiang Rai (northern Thailand) and 2 in Khon Kaen (northeastern Thailand). We enrolled patients >7 years of age with a temperature >38°C who were brought to study hospitals for treatment from February 4, 2002, through March 28, 2003. Patients were excluded if they had a history of fever for >2 weeks or an infection that could be diagnosed clinically. Acute-phase serum samples were collected at the time of enrollment and convalescent-phase serum samples 3–5 weeks later. We enrolled nonfebrile control patients >14 years of age who had noninfectious conditions; acute-phase serum samples were collected. Clinical information was abstracted from patient charts. Nurses conducted physical examinations and personal interviews to collect information on patients’ demographic characteristics, exposures to animals, and outdoor activities.

Serum samples were tested for immunoglobulin (Ig) G antibodies to Bartonella spp. by immunofluorescent antibody assay at the Bartonella Laboratory of the Centers for Disease Control and Prevention, Fort Collins, CO, USA. Strains used for antigen production were: B. elizabethae (F9251), B. henselae (Houston-1), B. quintana (Fuller), and B. vinsonii subsp. vinsonii (Baker). Homologous hyperimmune serum specimens were produced in BALB/c mice as previously described (8). Bartonella infection was considered confirmed in febrile patients who had a >4-fold rise in IgG antibody titers and a convalescent-phase titer >64. Probable infection was defined as 1) a 4-fold antibody titer rise but convalescent-phase titers of 64, or 2) high and stable titers (>512 in acute-phase and convalescent-phase serum samples), or 3) acute-phase titer >512 with a >4-fold titer fall. Paired serum samples from febrile patients were also tested for serologic evidence of other common causes of febrile illness in Southeast Asia.

Febrile patients with acute-phase and convalescent-phase IgG antibody titers <128 were considered not to have Bartonella infection; we compared demographic and clinical characteristics of these patients to Bartonella-infected patients. To evaluate potential risk factors, we compared Bartonella-infected case-patients >14 years of age without serologic evidence of other infections (n = 20) to nonfebrile controls with IgG to Bartonella <128 (n = 70). Age adjusted odds ratios (AORs) with 95% confidence intervals (CIs) were calculated.

Benoit VM, Petrich A, Alugupalli KR, Marty-Roix R, Moter A, Leong JM, Boyartchuk VL.

Department of Molecular Genetics and Microbiology, and Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605; Institut für Mikrobiologie und Hygiene, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, 10117 Berlin, Germany; Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107.

Host susceptibility to infection is controlled in large measure by the genetic makeup of the host. Spirochetes of the genus Borrelia include nearly 40 species of vector-borne spirochetes that are capable of infecting a wide range of mammalian hosts, causing Lyme disease and relapsing fever. Relapsing fever is associated with high-level bacteremia, as well as hematologic manifestations such as thrombocytopenia (i.e. low platelet numbers) and anemia. To facilitate studies of genetic control of susceptibility to Borrelia hermsii infection we performed a systematic analysis of the course of infection using immunocompetent and immunocompromised inbred strains of mice. Our analysis revealed that sensitivity to B. hermsii infections is genetically controlled. In addition, whereas the role of adaptive immunity to relapsing fever spirochetes is well documented, we found that innate immunity contributes significantly to reduction of bacterial burden. Similar to human infection, progression of the disease in mice was associated with thrombocytopenia and anemia. Histological and fluorescence in situ hybridization (FISH) analysis of infected tissues indicated that red blood cells were removed by tissue resident macrophages, a process that could lead to anemia. Spirochetes in the spleen and liver were often visualized associated with RBCs, lending support to the hypothesis that direct interaction of B. hermsii spirochetes with RBCs leads to clearance of bacteria from the bloodstream by tissue phagocytes.

PMID: 19995898 [PubMed – as supplied by publisher]

(HealthDay News) — Almost half of tested samples of commercial high-fructose corn syrup (HFCS) contained mercury, which was also found in nearly a third of 55 popular brand-name food and beverage products where HFCS is the first- or second-highest labeled ingredient, according to two new U.S. studies.

HFCS has replaced sugar as the sweetener in many beverages and foods such as breads, cereals, breakfast bars, lunch meats, yogurts, soups and condiments. On average, Americans consume about 12 teaspoons per day of HFCS, but teens and other high consumers can take in 80 percent more HFCS than average.

“Mercury is toxic in all its forms. Given how much high-fructose corn syrup is consumed by children, it could be a significant additional source of mercury never before considered. We are calling for immediate changes by industry and the [U.S. Food and Drug Administration] to help stop this avoidable mercury contamination of the food supply,” the Institute for Agriculture and Trade Policy’s Dr. David Wallinga, a co-author of both studies, said in a prepared statement.
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In the first study, published in current issue of Environmental Health, researchers found detectable levels of mercury in nine of 20 samples of commercial HFCS.

And in the second study, the Institute for Agriculture and Trade Policy (IATP), a non-profit watchdog group, found that nearly one in three of 55 brand-name foods contained mercury. The chemical was found most commonly in HFCS-containing dairy products, dressings and condiments.

More charming facts about high-fructose corn syrup

HFCS contains more fructose than sugar and this fructose is more immediately available because it is not bound up in sucrose. Since the effects of fructose are most severe in the growing organism, we need to think carefully about what kind of sweeteners we give to our children. Fruit juices should be strictly avoided–they are very high in fructose–but so should anything with HFCS…

…(Scientists conducted) studies with two groups of rats, one given high amounts of glucose and one given high amounts of fructose (the sugar found in corn syrup.)

The glucose group was unaffected but the fructose group had disastrous results.

The male rats did not reach adulthood. They had anemia, high cholesterol and heart hypertrophy–that means that their hearts enlarged until they exploded. They also had delayed testicular development.

Dr. Field explains that fructose in combination with copper deficiency in the growing animal interferes with collagen production. (Copper deficiency, by the way, is widespread in America.)

In a nutshell, the little bodies of the rats just fell apart. The females were not so affected, but they were unable to produce live young.

Source: http://www.westonaprice.org