Is There An Undetected Chagas Pandemic?

Chagas Disease: Poverty, Immigration, and the ‘New HIV/AIDS’:

The issue with Chagas isn’t only that its primary victims represent an undetected public health and healthcare burden; when they do not know they are infected, they can become a source of infection as well. The protozoan can pass from mother to child during pregnancy, causing congenital Chagas; and when infected people donate blood or become organ donors, the protozoan hitches a ride. The earliest cases of Chagas in New York City, back in the 1980s, were transmitted by transfusion. There’s been an FDA-approved test for Chagas in donated blood for just two years. The latest map from AABB (formerly the American Association of Blood Banks), showing where positive donations have been identified, vividly demonstrates how the disease has spread.

… A third paper, published two years ago in PLoS NTD, argues that Chagas is now endemic in Texas, traveling from Triatoma species through dogs and into people — and is going undetected because blood-donation screening is not mandatory in the state and physicians are not required to report the disease’s occurrence to health authorities. (Chagas in fact is only reportable in a handful of states.) …

When I read "new HIV/AIDS" and "undetected" in the context of pathogens, I become reminded of the XMRV fraud creative accounting by Mikovits/Ruscetti. The whole fear-mongering is just so similar to XMRV. And the reckless compassionate "Chronic Lyme" diagnosis by so called "Lyme Literate Medical Doctors (LLMD)" comes to my mind.

But then again, there might actually be an Chagas pandemic. And I know how ME/CFS has been treated by the health authorities.

And the AABB results are different from the XMRV wild goose chase – there seems to actually be something to find, unlike XMRV.

I wonder how many more "undetected" disease are out there…

NIAID on Chronic Lyme and long-term Antibiotic use

NIAID on Chronic Lyme:

The first clinical trial, which included two studies conducted at multiple research sites, provided no evidence that extended antibiotic treatment is beneficial (New Engl J Med 345: 85-92, 2001). In those studies, physicians examined long-term antibiotic therapy in patients with a well-documented history of previous Lyme disease, but who reported persistent pain, fatigue, impaired cognitive function, or unexplained numbness. Patients were treated with 30 days of an intravenous antibiotic followed by 60 days of treatment with an oral antibiotic.

These studies did reinforce the evidence that patients reporting PLDS symptoms have a severe impairment in overall physical health and quality of life. However, prolonged antibiotic therapy showed no benefit when compared with groups who received placebo.

In another study, published in 2003, researchers examined the effect of 28 days of intravenous antibiotic compared with placebo in 55 patients reporting persistent, severe fatigue at least 6 months following treatment for laboratory-diagnosed Lyme disease. Patients were assessed for improvements in self-reported fatigue and cognitive function (Neurology 60: 1923-30, 2003).

In that study, people receiving antibiotics did report a greater improvement in fatigue than those on placebo. However, no benefit to cognitive function was observed. In addition, six of the study participants had serious adverse events associated with intravenous antibiotic use, and four patients required hospitalization. Overall, the study authors concluded that additional antibiotic therapy for PLDS was not supported by the evidence.

More recently, a study supported by the National Institute of Neurological Disorders and Stroke (NINDS), also a part of the National Institutes of Health, again showed that long-term antibiotic use for Lyme disease is not an effective strategy for cognitive improvement (Neurology 70(13): 992-1003, 2008). Researchers compared clinical improvement following 10 weeks of intravenous ceftriaxone versus intravenous placebo. The patients were treated for Lyme disease and presented with objective memory impairment tests. In a complicated statistical model, the ceftriaxone group showed a slightly greater improvement at 12 weeks, but at 24 weeks, both the ceftriaxone and the placebo groups had improved similarly from baseline. In addition, adverse effects attributed to intravenous ceftriaxone occurred in 26 percent of patients. The authors concluded that because of the limited duration of the cognitive improvement and the risks involved, 10 weeks of intravenous ceftriaxone was not an effective strategy for cognitive improvement in these patients, and more durable and safer treatment strategies are still needed.

To recap:

• The people are ill 
• Long-term antibiotics do most certainly not cure
• Long-term antibiotics have dangers
• Diagnose is done through "a well-documented history of previous Lyme disease"

As far as I am concerned, there is no evidence that "Chronic Lyme" or "post-Lyme disease syndrome" (PLDS) is anything else then just another pathogen that can cause CF(S) or PVFS.

"It’s Not so Rare to Have a Rare Disease"

Spittoon – It’s Not so Rare to Have a Rare Disease

When we think about diseases we often describe them as either common or rare. Common conditions — like heart disease and obesity — are complex in nature, meaning that they are influenced by both genetics and environment. Conversely, most rare diseases are strongly influenced by genetics and less so by environment. We hear a lot about common conditions because so many people have them and in contrast relatively little about rare diseases. But how rare is rare?

In the United States, a disease is defined as “rare” if it affects fewer than 200,000 individuals, or roughly one in 1500. Rare diseases are often poorly understood, with symptoms that can be difficult to diagnose, and can be life-threatening. Around 6,800 rare diseases have been identified and the large majority of them — up to 80% — are thought to have a genetic origin. Most rare diseases can’t be cured and many lack effective treatments because research on rare conditions is often hampered by a scarcity of study participants and poor funding.

If you add up all the rare diseases it turns out that about 30 million Americans suffer from a rare disease. That’s nearly 10% of the population — suddenly rare is not so rare! …

Well, they sell genetic tests, so they have toot their horn. But still: 10% have a "rare" disease. Wow.

"Multiple Chemical Sensitivity (MCS): A Spurious Diagnosis"

Stephen Barrett, M.D. at Quackwatch on Multiple Chemical Sensitivity ("MCS"):

…
Psychologist Herman Staudenmayer, Ph.D., of Denver, Colorado, has treated "MCS" patients for more than 30 years. He believes that although some people are very sensitive to various microorganisms, noxious chemicals, and common foods, there is no scientific evidence that an immunologic basis exists for generalized allergy to environmental substances. During the 1990s, like Rea, Staudenmayer and his colleague—the late John C. Selner, M.D. (an allergist)—used an environmental chamber to test sensitivity to airborne chemicals. However, they rejected clinical ecology theories and practices. Using well-designed double-blind tests, they demonstrated that "universal reactors" may develop multiple symptoms in response to the testing process without being allergic to any of the individual substances administered. One of their reports describes how they used an environmental chamber to evaluate 20 patients with multiple symptoms attributed to chemical hypersensitivity. These patients believed that they were reactive or hypersensitive to low-level exposure to many chemicals. Some had previously been evaluated and managed by clinical ecologists and diagnosed with "MCS." During nonblinded tests, these patients consistently reported symptoms they had associated with exposure at work, at home, or elsewhere. The environmental chamber enabled the patients to encounter measured amounts of purified air, compressed gasses, and air containing specific chemical concentrations, without knowing which situation was which. None of the patients demonstrated a response pattern implicating the chemicals supposedly responsible for their symptoms. Eighteen reported no symptoms at least once when the suspect chemical was present. Fifteen reported symptoms at least once when the suspect chemical was absent [10]. In other words, patients reacted to their feelings and beliefs about the test, rather than to the substance in question [11].

In 1999, the American Health Foundation's Environmental Health and Safety Council reached a similar conclusion. After reviewing the evidence for various alleged mechanisms though which odor-bearing chemicals might cause MCS symptoms, the council concluded:

In no case was there persuasive evidence that any olfactory mechanism involving fragrance underlies either induction of a sensitized state or the triggering of MCS symptoms. Fragrances and other odorants could, however, be associated with symptoms as claimed by MCS symptomatics, because they are recognizable stimuli, but fragrance has not been demonstrated to be causal in the usual sense. [12]

A more recent study tested whether "MCS" patients could reliably distinguish between airborne solvents and placebo and whether there were significant differences in measurable biological and neuropsychological parameters between solvent and placebo exposures. During the study, 20 MCS patients and 17 controls underwent six sessions in a challenge chamber in which they were exposed to solvent fumes and clean air in random order. Neither the patients nor the experimentors knew which exposures were which at the time they took place. No differences accuracy in identifying chemical exposure were found between the two groups. Nor was cognitive performance influenced by solvent exposure or different between the groups. Nor was there any difference between the groups in serum cortisol levels measured before and after exposures [13].

So probably no MCS, but other illnesses.

So what about the symptoms? They are interesting:

… The complaints associated with these labels include depression, irritability, mood swings, inability to concentrate or think clearly, poor memory, fatigue, drowsiness, diarrhea, constipation, dizziness, mental exhaustion (also called "brain fog" or "brain fag"), lightheadedness, sneezing, runny or stuffy nose, wheezing, itching eyes and nose, skin rashes, headache, chest pain, muscle and joint pain, urinary frequency, pounding heart, muscle incoordination, swelling of various parts of the body, upset stomach, tingling of the fingers and toes, and psychotic experiences associated with schizophrenia.

Well, some of it sounds like from ME/CFS, Fibromyalgia and POTS…

William J. Rea, M.D., who says he has treated more than 20,000 environmentally ill patients, states that they "may manifest any symptom in the textbook of medicine."

Oh my. If someone can diagnose literally anyone with MCS for having "any symptom in the textbook of medicine", then MCS is a worthless diagnose. And most certainly one will miss many other diagnoses, of real illnesses and diseases.

How endogenous retroviruses fuck up the immune-system

The endogenous guys are also berry sneaky. While they are no longer completely functional they still can transcribe-->translate a superantigen. Its a viral protein, but because it is expressed before the immune system matures, the immune system recognizes the viral protein as 'self.' That means that all the T-cells that would kill an MMTV infected cell are killed, like all T-cells that recognize 'self' proteins. Mice basically lose an arm of their immune system.

Remember the classes of T-Cell Receptors I was talking about with the possums? Endogenous MMTVs (and the infection of pups before their immune system matures) can cause the loss of all T-cells that have certain Variable Beta chains. This deletion increase the mouses susceptibility to new MMTV infections, and also increases susceptibility to other pathogens, like cholera. Yup-- A virus screwing around with how well you can fight off bacteria.

It took 30 years to find out what causes hemolytic uremic syndrome

As I've laid out this week, the realization that a fairly simple, toxin-carrying bacterium could cause a "complex" and mysterious disease like hemolytic uremic syndrome came only with 30 years' of scientific investigation and many false starts and misleading results. Like many of these investigations, the true cause was found due to a combination of hard work, novel ways of thinking, and simple serendipity--being able to connect the dots in a framework where the dots didn't necessarily line up as expected, and removing extraneous dots as necessary. It's not an easy task, particularly when we've had mostly culture-based methods to rely on since the dawn of microbiology. (via)

Leukemia caused by an infection?

Both Kinlen’s ‘population-mixing’ hypothesis and Greaves ‘delayed infection’ hypothesis summarize the considerable evidence that childhood leukemia may be the consequence of an abnormal response to a common or uncommon infection(s).

From:
Unusual space-time patterning of the Fallon, Nevada leukemia cluster: Evidence of an infectious etiology (via)