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Full article: http://www.cidrap.umn.edu/cidrap/content/influenza/swineflu/news/jul2110newsscan.html 

Excerpt:

Among new tick-related infectious disease findings presented at the International Conference on Emerging Infectious Disease (ICEID), which ended Jul 14 in Atlanta, were a report on the first zoonotic babesiosis case documented in Tennessee and a report on ehrlichiosis infections in Minnesota and Wisconsin involving a species that had not previously been identified in North America. In the first report, a group from the Tennessee Department of Health, Vanderbilt University, and the CDC diagnosed babesiosis in an immunosuppressed patient who began to have fever, fatigue, and headache. He had not traveled outside Tennessee in several years and had been exposed to ticks during hunting trips. Babesia parasites were noted on the man’s blood smear, and molecular analysis revealed that it was a novel species, but attempts to isolate it were unsuccessful. The man’s symptoms resolved after 10 days of treatment. The researchers said efforts to identify the animal host and tick vectors are ongoing and that the case serves as a reminder that patients can have babesiosis without exposure to known endemic areas and without testing positive to previously known species. In the second report, local health officials and CDC and Mayo Clinic experts described the identification of Ehrlichia DNA from Mayo Clinic blood samples of patients from the two states involving a species similar to E muris that had not been previously identified in North America. The organism was found in 2009 in the blood of 4 patients, 3 from Wisconsin and 1 from Minnesota. All had reported fever and headache, and all had lymphopenia. All recovered with doxycycline treatment. Serological studies also suggested 40 more probable cases among Wisconsin residents. A survey of the patients found dog contact in 91% and possible tick exposure in 85%. The group concluded that more studies are needed to identify the epidemiologic and clinical features of infections with the E muris–like organism and that better testing in the region could help identify the infections.

Excerpt:

89 cases of neuroborreliosis were reported; in 66 cases diagnosis was confirmed. Facial weakness was one of the presenting symptoms in 47 cases (71%) and the only symptom in nine children (14%). The five complaints most frequently reported were: malaise, headache, fatigue, fever and neck pain. 52 children (79%) had one or more objective neurological signs at presentation, of which facial nerve palsy, other cranial nerve abnormalities and meningeal signs were most frequent. 14 patients (21%), however, had no neurological signs at physical examination. In these patients, the number of subjective complaints was higher, and the time interval to diagnosis was longer compared with those with objective neurological abnormalities.

Conclusions

In this study, 79% of paediatric neuroborreliosis patients presented with neurological signs, most often facial nerve palsy. 21% presented in an atypical way without neurological signs. A thorough neurological examination is essential once neuroborreliosis is considered in children. Even in the absence of neurological signs, neuroborreliosis may be suspected in children with typical antecedents and multiple symptoms. Cerebrospinal fluid investigations are then required to confirm the diagnosis.

Full article: http://www.biomedcentral.com/1471-2334/10/229

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.

Full article: http://www.smh.com.au/nsw/court-grants-lyme-disease-autopsy-20100719-10hyx.html

Excerpt:

A SYDNEY woman has been awarded a Supreme Court injunction to have her dead husband tested for a disease the Health Department says does not exist in Australia.

Mualla Akinci’s husband, Karl McManus, died last Wednesday – three years after he was bitten by a tick she says carried Lyme disease, a bacterial infection which, if left untreated, can cause profound neurological damage.

Mr McManus, 43, from Turramurra, was bitten on the left side of his chest during filming for the television show Home and Away in bushland in Waratah Park, northern Sydney. Within six weeks he lost mobility in one of the fingers on his left hand. That quickly spread to paralysis in his left arm and across to his right arm.

Mr McManus was diagnosed with multifocal neuropathy after testing negative for Lyme disease, but Ms Akinci, a pharmacist, insisted he be tested again at clinics in the US and Germany. Both tests returned positive for Lyme disease.

She argues that Australian tests are inadequate because pathologists looks for antibodies in the blood, rather than for proteins in specific bacteria within tissue.

”Lyme doesn’t usually live in the blood. It lives in tissues unless someone’s system is flushed with it so it stands to reason that every test will come back negative,” Ms Akinci said.

The Health Department maintains that no case has been transmitted in Australia and the organisms that cause it – three species of the genus borrelia – are not carried here by wildlife, livestock or their parasites.

The NSW Health Minister, Carmel Tebbutt, said in May there was not enough evidence to support the existence of ticks carrying the borrelia organism.

”Until there is solid evidence to indicate that locally acquired Lyme disease is a significant public health matter in Australia, specific measures to educate the general public or clinicians are difficult to justify,” she said.

Full article: http://ukpmc.ac.uk/articles/PMC1490240;jsessionid=7D7D2D45FB70B5A24793992EDD921DFB.jvm4

Excerpt:

Abstract

A case of 65-year-old male is reported who presented with myalgias, headache, and fever. He subsequently developed myocarditis and was diagnosed to have anaplasmosis on peripheral blood smear. He was treated with doxycycline for 30 days. A coronary angiogram done after recovery showed normal epicardial arteries. The case illustrates the importance of a careful examination of the peripheral smear, with a high index of clinical suspicion, which led to prompt treatment and complete recovery of the patient

Ehrlichiosis, first discovered before 1910, has been recognized to cause human infection since 1986.1 It belongs to Rickettsiaceae family. Ehrlichiae are small, obligate intracellular bacteria that grow in cytoplasmic vacuoles to form clusters called morulae. Three distinct species cause human ehrlichiosis. E. chaffeensis predominantly affects the monocytes and is hence termed human monocytic ehrlichiosis (HME) while E. phagocytophilium, and E. ewingii cause human granulocytic ehrlichiosis.2E. phagocytophiliumE. equi are now recognized as the same organism and has been renamed Anaplasma phagocytophilum; the disease is now known as Human Granulocytic Anaplasmosis (HGA). Both HME and HGA share similar clinical and laboratory features and are treated with the same antimicrobials.

  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
 

Linda’s comments:  Tick population exploding isn’t just on the East coast, it is US wide.  More and more ER’s are reporting a BIG increase with tick bites.   More importantly, you don’t have to have a tick bite to get Lyme disease.  BEWARE and pay attention when in the great outdoors.

Full article: http://www.newburyportnews.com/punews/local_story_099222830.html

Excerpt:

NEWBURYPORT — Deer ticks have been appearing in huge numbers throughout the region, raising concerns about Lyme disease.

All along the East Coast, health experts have seen a sudden and dramatic increase in ticks.

“Just in the past week or two, we have seen an explosion in deer ticks,” said Dr. Heidi Bassler, medical director of the Veterinary Center of Greater Newburyport.

The unusually warm weather and record-setting rains have helped bolster the tick population. Hospitals, such as Addison-Gilbert in Gloucester, have experienced a surge in tick bite cases. Normally, the hospital sees one or two cases per day; now it is seeing eight or 10.

There are two different kinds of ticks that are predominant in the region. Dog ticks are about the size of a pencil eraser; deer ticks, the more dangerous species, are closer to the size of a pen point.

With a single bite, deer ticks can transmit Lyme disease, symptoms of which include a debilitating complex of fever, headache, fatigue and depression, and two other illnesses of similar symptoms.

Ticks are mostly found in woods and fields. High grass, including dune grass, is one of their favored habitats.

Volume 16, Number 4–April 2010

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.

Full article: http://www.lymeneteurope.org/forum/viewtopic.php?f=7&t=1336#p9502

Excerpt:

Abstract
Using PCR in conjunction with pre-enrichment culture, we detected Bartonella henselae and B. vinsonii subspecies berkhoffii in the blood of 14 immunocompetent persons who had frequent animal contact and arthropod exposure.

Attempts to isolate Bartonella sp. from immunocompetent persons with serologic, pathologic, or molecular evidence of infection are often unsuccessful; several investigators have indicated that Bartonella isolation methods need to be improved (1–4). By combining PCR and pre-enrichment culture, we detected B. henselae and B. vinsonii subspecies berkhoffii infection in the blood of immunocompetent persons who had arthropod and occupational animal exposure

The Study

From November 2004 through June 2005, blood and serum samples from 42 persons were tested, and 14 completed a questionnaire, approved by the North Carolina State University Institutional Review Board. Age, sex, animal contact, history of bites, environment, outdoor activity, arthropod contact, travel, and medical history were surveyed. Bacterial isolation, PCR amplification, and cloning were performed by using previously described methods (5–7). Each blood sample was tested by PCR after direct DNA extraction, pre-enrichment culture for at least 7 days, and subculture onto a blood agar plate (Figure). An uninoculated, pre-enrichment culture was processed simultaneously as a control. Methods used for DNA extraction and conventional and real-time PCR targeting of the Bartonella 16S-23S intergenic spacer (ITS) region and heme-binding protein (Pap31) gene have been described (7,8). Conventional PCR amplicons were cloned with the pGEM-T Easy Vector System (Promega, Madison, WI, USA); sequencing was performed by Davis Sequencing, Inc. (Davis, CA, USA). Sequences were aligned and compared with GenBank sequences with AlignX software (Vector NTI Suite 6.0 (InforMax, Inc., Bethesda, MD, USA) (7,8). B. vinsonii subsp. berkhoffii, B. henselae, and B. quintana antibodies were determined by using a modification of a previously described immunofluorescence antibody assay (IFA) procedure (9

Study participants included 12 women and 2 men, ranging in age from 30 to 53 years; all of them reported occupational animal contact for >10 years (Table). Most had daily contact with cats (13 persons) and dogs (12 persons). All participants reported animal bites or scratches (primarily from cats) and arthropod exposure, including fleas, ticks, biting flies, mosquitoes, lice, mites, or chiggers. All participants reported intermittent or chronic clinical symptoms, including fatigue, arthralgia, myalgia, headache, memory loss, ataxia, and paresthesia (Table). Illness was most frequently mild to moderate in severity, with a waxing and waning course, and all but 2 persons could perform occupational activities. Of the 14 participants, 9 had been evaluated by a cardiologist, 8 each by an infectious disease physician or a neurologist, and 5 each by an internist or a rheumatologist. Eleven participants had received antimicrobial drugs.