re: Why do you think that TD is such a magnet for those with alternative beliefs?

No experimental proof of aerosol human to human transmission of any disease. That is far more than enough. Your theories sound great but have no basis.

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Then, develop alternative theories.

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So, as I asked you before, what are these alternative "theories" and what evidence do you have to support them?

So, as I asked you before, what are these alternative "theories" that explain the underlying phenomena and what evidence do you have to support them?

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No experimental proof of aerosol human to human transmission of any disease. That is far more than enough. Your theories sound great but have no basis.

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Okay, you have to stop using 'aerosol.' It doesn't mean anything

But they do have basis and have been proved clinically. Pathogens show characteristic patterns of disease at several levels. Hypothesis are proposed on how to treat the illness and the patient gets better. Repeat this ad nauseum several hundreds of thousands of times in hundreds of settings. The scientific method is literally built into how physicians approach pathophysiology. Most importantly, these avenues provide falsifiability. In extremely sterile environments, we had patients who were under airborne and droplet precautions get opportunistic infections. How did that occur?

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They actually cause symptoms, which is interesting because symptoms are usually framed as the body's immune response to the pathogen

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You aren't understanding what I'm saying here. Pathogens cause characteristic patterns of disease at the molecular level. They have characteristic entry methods, immune defenses and morphologies. The fact that I can use a medication that has a narrow focus and successfully treat a patient is a type of repeatable experiment, one that has millions of data points. Like I said, the floors do not lie. If during a physical exam, I noticed that a patient has dullness on percussion and diminished breath sounds from yesterday, and on CXR I see fibrocaseous cavitary lesions on the upper lobes, I know I'm dealing with postprimary TB. If I can get a sample and it is sensitive to initial therapy with RIPE and the patient is started on that and sees improvement, what am I supposed to assume? I had some observable finding on physical, I ordered a CXR to investigate, I obtained the samples and I started a treatment, which worked. What else am I supposed to assume here?

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That kind of proves my point, doesn't it? I think your whole thinking about infections and pathogens is foundationally wrong.

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It doesn't. Think this through. You have pathogens as part of your skin, gut, and mucosal tissue that exist as part of the natural flora. Even under strict precautions, they can get sick in immunosuppressed states just from something as simple as moving their hands to their nose or feeding themselves. How do we know that? Because there are few characteristic opportunistic pathogens that present in extremely similar ways, enough that we can categorize them as diseases. How was HIV first detected? The first reports in the 80's were not from discussions about the isolation of the pathogen, but from the extremely rare characteristic infection that developed in a certain subset of the population.

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They have characteristic entry methods, immune defenses and morphologies. 

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Why are they doing that? How do you know they are a malicious living parasite, wishing to jump from person to person, reproduce and thrive inside their host they may eventually kill?

There is no proof of their transmission. You can't give it to someone and make them sick, it's never been done. How do you know their intent? WHY do they present? How do you know, conclusively, they are not synthesized or acquired by the living body as a response to diseased tissue?

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Why are they doing that?

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Why are they doing what?

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How do you know they are a malicious living parasite, wishing to jump from person to person, reproduce and thrive inside their host they may eventually kill?

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Because we can isolate them from patient tissue samples. Not all pathogens respond to the same type of staining, and upon staining, each pathogen has its own pattern of cellular injury. Broadly, the patterns of molecular injury show up in characteristic signs, which occur often enough with the appearance of pathogens on sputum that we can safely assume, from millions of data points, that those pathogens are the cause of those injuries.

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There is no proof of their transmission.

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Of any disease?

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You can't give it to someone and make them sick, it's never been done.

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So if I stick you with a needle from a person infected with HIV, you wouldn't get HIV?

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How do you know their intent?

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Why does that matter?

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WHY do they present?

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Do you mean, why do different diseases have different presentations and become associated with specific signs, symptoms and characteristics?

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How do you know, conclusively, they are not synthesized or acquired by the living body as a response to diseased tissue?

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Because of several million data points which involve the collection of tissue samples. We know they aren't synthesized by the body because of characteristic patterns of injury. With TB we will see central granular caseation in lung-tissue surrounded by epithelioid and giant cells. Occasionally these granulomas may not show central caseation, but when granulomas appear, we can confirm the presence by acid-fast organisms through special stains, which confirms infection. For fungal infections we can do the same thing with respect to the lung, especially if acid-fast stains produce nothing, at which point we can move to silver stains, which again will show characteristic granulomas. Histoplasmosis yeast forms will fill phagocytes in a lymph node, while Coccidioidomycosis will show intact yeast spherules within multinucleated giant cells. Blastomycosis will show rounded budding yeasts with a characteristic thickened wall and nuclei. We can differentiate PJP by its foamy exudate that appears pink with a hematoxylin-eosin stain, while silver staining reveals round or cup-shaped cysts within alveolar exudates. Healthy tissue subjected to these stains will not likely produce characteristic patterns associated with infectious disease. They might show other disease patterns, which is how we can differentiate an autoimmune response, which also has its own characteristic pattern of injury, from an environmental response to an infectious injury patterns.

Most of all, we can see the difference after we find an infection and treat the pathogen specifically. That type of testable hypothesis is repeated so many times that no one thinks to characterize it in terms of a defense of germ theory. Again, the floors don't lie. The clinical aspect of medicine has results which act like data points across a population. You need justifications, evidence, samples, pathology, tests, etc. in order to have a treatment plan followed.

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Because we can isolate them from patient tissue samples. Not all pathogens respond to the same type of staining, and upon staining, each pathogen has its own pattern of cellular injury. Broadly, the patterns of molecular injury show up in characteristic signs, which occur often enough with the appearance of pathogens on sputum that we can safely assume, from millions of data points, that those pathogens are the cause of those injuries.

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They are present in the sputum, they have characteristics of cell injury. Now how did they get in the sick person's sputum? It's not from an airborn sneeze as far as I can tell. How did they get there?

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Of any disease?

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no proof of aerosol human to human transmission of any disease

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So if I stick you with a needle from a person infected with HIV, you wouldn't get HIV?

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I'd probably get something

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Do you mean, why do different diseases have different presentations and become associated with specific signs, symptoms and characteristics?

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ASSOCIATION IS NOT CAUSE.

Is a stomach bug caused by the color green?

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We know they aren't synthesized by the body because of characteristic patterns of injury. 

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Explain. You believe in other autoimmune characteristics. Why does their pattern of injury conclusively preclude the possibility of synthesization?

Yeast is a fungus. I may believe in fungal infection. I will be more specific with pathogens, namely purportedly-airborn-transmitted bacteria and viruses.

There is no proof of their airborn transmission causing disease between humans. Consistent presence and characteristics of cell injury do not rule them out as an immune response. They raise the possibility. There is no proof against that theorem, and no proof they are airborn transmissible.

A poorly understood autoimmune response is plausible. Especially with the complete lack of hard evidence for airborn transmission

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They are present in the sputum, they have characteristics of cell injury. Now how did they get in the sick person's sputum? It's not from an airborn sneeze as far as I can tell. How did they get there?

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Well it depends on the pathogen. If we know that TB has a characteristic pattern of injury, and we know that it generally doesn't survive on any surfaces or human skin, what can we safely assume?

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Is a stomach bug caused by the color green?

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There are stomach bugs that have characteristic signs of injury and will produce characteristic symptoms. If we see progression of diarrhea from watery to bloody in the setting of severe abdominal pain, vomiting, fever, that limits our pathogenic options. And if we start seeing thrombocytopenia along with acute kidney injury, that also leads us to a likely conclusion, which can be confirmed by schistocytes on blood smear. You would immediately suspect Hemolytic Uremic Syndrome caused E. coli 0157:H7, though you couldn't necessarily rule out Shigella dysenteriae type 1, depending on the population profile. You have to take in the whole constellation at once, not just a small piece.

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Explain. You believe in other autoimmune characteristics. Why does their pattern of injury conclusively preclude the possibility of synthesization?

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Autoimmune disease will generally show different cellular injury patterns, which are usually some type of immune complex. Those are further differentiated into specific types of hypersensitivies which have histopathologic lesions which are different from one another. Type 3 would see antigen-antibody complexes deposited in specific tissues, while Type 2 will see IgG or IgM bound-antigens deposited in the mesangial matric as in Goodpasture, where on trichrome staining you will see collagen deposits with glomerular capillaries that are stained blue, fibrin deposits within the renal corpuscle that represent fibrin, which shows that there a leakage that is occurring in the glomerular capillary loops into the urinary space. You will also see a crescent formed by deposition of fibrin with macrophages and proliferated parietal cells of the Bowman's capsule. On immunofluorescence you will see the IgG antibody deposition. If you stained these slides looking for a pathogen, you would not likely find one.

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Yeast is a fungus. I may believe in fungal infection. I will be more specific with pathogens, namely purportedly-airborn-transmitted bacteria and viruses.

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But fungal infections that are systemic are mainly limited to opportunistic pathogens in the immunosuppressed. They are much less common over a population.

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There is no proof of their airborn transmission causing disease between humans.

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The clinical side is overwhelming in evidence.

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Consistent presence and characteristics of cell injury do not rule them out as an immune response.

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They generally do, because immune response occurs along a cascade of very specific cells and proteins which allow for immune function. Indeed, some of those cellular patterns include macrophages which are included within pathogen-specific cellular injury. But here you need to understand how the immune system works. It works through the recognition of PAMPs, which are pathogen associated molecular patterns, the recognition of which starts the immune process. Sometimes we see bacteria that have type III secretion systems that inject bacterial proteins into the host cytosol to manipulate host function. You can be extremely specific once you understand the molecular level interactions. There's no way to mistake the patterns of cellular injury in both the specific sense at the molecular level and within the constellation of symptoms that are produced.

Autoimmune disorders also occur within a constellation of symptoms too, which are different from symptoms associated with infectious disease. You wouldn't mistake sarcoidosis for tuberculosis because they exist within the setting of other symptoms, even though the initial before-HPI and exam presentation might be similar. It's why there is a systematic process in place that is used over and over to differentiate diseases from one another.

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A poorly understood autoimmune response is plausible. Especially with the complete lack of hard evidence for airborn transmission

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It genuinely isn't, because immune cascades are going to be extremely, and I mean, extremely specific. They are so specific we've narrowed them down to four broad categories of hypersensitivies. They will have meaningfully different exam, lab, and diagnostic findings in the setting of meaningfully different symptoms. That's the part you are not understanding.

Fair enough.

I do appreciate reading the information though, and there is some amusement in someone that clearly doesn't know what the frick he is talking about trying to argue a doctor and not realize how poorly he's doing at it