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Communicable (contagious) diseases are carried by microorganisms and transmitted through people, animals, surfaces, foods, or air. Communicable diseases rely on fluid exchange, contaminated substances, or close contact to travel from an infected carrier to a healthy individual.

Parasites, bacteria, and viruses all qualify as pathogens, nicknamed "germs," and can cause a communicable disease. Their method of transmission, period of dormancy, ease of contagiousness, and relative danger can differ drastically from one disease to the next.
 
Infectivity
 
The term infectivity describes the ability of an organism to enter, survive and multiply in the host. Infectiousness of a disease indicates the comparative ease with which the disease is transmitted to other hosts.
 
Infectivity and infectiousness are characteristic of virulence. Virulence refers to the degree of pathogenicity of an organism, or in other words the relative ability of a pathogen to cause disease.
 
Among the almost infinite varieties of microorganisms, relatively few cause disease in otherwise healthy individuals. Infectious disease results from the interplay between those few pathogens and the defenses of the hosts they infect. The appearance and severity of disease resulting from any pathogen depends upon the ability of that pathogen to damage the host as well as the ability of the host to resist the pathogen.
 
Transmission
 
Patients should not be overly concerned about their communicability. Everyone is exposed to Th1/Th17 pathogens in a variety of ways because these L-form bacteria are everywhere. They’re in our food/milk (they’re not killed by pasteurization), water (they’re not killed by fluoridation), and biologic (injectible) medicines (they’re too small to be filtered during the 'purification' processes used in pharmaceutical manufacturing procedures).
 
Th1/Th17 pathogens form a microbiota (community) which is part of the human existence. If they don’t cause disease when a person is young, it’s believed they will ultimately cause the diseases of aging, and the processes of aging. Acquiring these pathogens is inevitable.
 
Patients with chronic Th1/Th17 inflammatory illnesses need not limit contact with the general public. Transmission of these bacteria requires close contact and is seen most often within the family unit.
 
It’s believed that once the amount of Inflammation Therapy antibiotics goes above the MIC (minimum inhibitory concentration) needed to kill opportunistic blood-borne bacteria there is little chance of passing intracellular bacteria to another person because the bacteria will be killed within 48 hours of leaving the cells and entering the bloodstream.
 
Before that point, the usual precautions taken to prevent the spread of disease are adequate.
 
Someone not on IT, who is symptomatic with Th1/Th17 disease, has a heavy TH1/Th17 pathogen load. Theoretically, those bacteria could be passed to someone else by close contact through bodily fluids such as coughing or sneezing and other intimate contact. The biggest study of sarcoidosis in history, the National Institutes of Health (NIH) 6-year ACCESS study, found that the risk for sarcoidosis, a Th1/Th17 inflammatory disease, increased nearly 5-fold in parents and siblings with the disease.
 
Dr Garth Nicholson's studies on chronic fatigue syndrome and autism and Gulf War Syndrome, found that 70% or more of family members were infected at 10 years after their fathers returned from Iraq. But 10 years indicates these intracellular bacteria grow very slowly and should be easy to kill before they overcome the immune system if IT is used. Once on IT, these Th1/Th17 bacteria will be killed faster than they can multiply.
 
Rise in the incidence of Th1/Th17 inflammatory diseases
 
The balance between intracellular pathogens and human co-existence has been upset and there has been a rapid and steady increase in Th1/Th17 inflammatory and ‘autoimmune’ disease in the USA since the 1960s. That increase is projected to continue, with the Centers for Disease Control (CDC) saying that one in every two of today's high school seniors will have diabetes by 2050.
Certain key events which are believed to be driving this epidemic:
  • Availability and widespread use, of beta-lactam antibiotics which promote the bacterial transition to intracellular forms 
     
  • The adoption of compulsory, mass vaccinations which can introduce intracellular bacteria into the body
     
  • The popularity of sun-bathing (i.e., light-skinned residents of sun-drenched nations have traditionally been fully clothed) which contributes to vitamin D metabolism dysregulation.
     
  • The immunosuppressive effect of vitamin D supplementation in baby foods (e.g., Nestle initiated a campaign to push synthetic vitamin D in baby formula in the late 1940s and 1950s) and the general food supply.
Community outbreaks of Th1/Th17 disease
 

If accurate diagnosis occurs due to a change in a medical community's acceptance of Th1/Th17 pathogens, it would appear as though there's an epidemic of Th1/Th17 disease .An outbreak of certain pathogens (e.g., Borrelia and Rickettsia) could cause an increase in symptoms due to subclinical intracellular infection because there is generally a point at which the body can no longer cope.


Family members
 
Patients who have taken proactive measures to find a way to recover from Th1/Th17 illness have given family members an important 'heads-up' about Th1/Th17 inflammation. Many clinical symptoms are not recognized by doctors as being due to inflammation and many inflammatory diseases are not diagnosed until they are quite advanced.
 
The symptoms of Th1/Th17 inflammation are insidious and people often come to think of them as normal. But they reduce the quality of life and can be causing silent damage to organs. Many patients who have a Th1/Th17 disease diagnosis and now realize that familial aggregation is a factor are looking more closely at their family members and recognizing 'warning flags' of Th1/Th17 symptoms.
 
The D-Metabolites tests are simple and may indicate if symptoms are due to Th1 inflammation. Because IT is so safe, its use is warranted if these tests are abnormal even if the patient does not have an official Th1 disease diagnosis. A therapeutic probe can be done based on inflammatory symptoms alone. See Therapeutic Probe.
 
Recognizing and effectively treating Th1/Th17 inflammation in its early stages is something that most patients were not lucky enough to do. But their children and other family members now have an early warning. Many patients are urging their family members not to wait until they feel worse. They’re asking their doctors to use the D-metabolites test to diagnose Th1/Th17 inflammation and consider IT if warranted.
 
Th1/Th17 inflammation is subclinical until symptoms appear and then symptoms are often discounted. Health is a relative term. Some persons who are apparently healthy may be harboring L-form bacteria. Adults family members of chronically ill patients who want to be sure they do not have systemic Th1/Th17 inflammation, should ask their doctor to test D-metabolites and/or allow a therapeutic probe with IT.
 
If other family members are positive for bacterial infections and/or are Th1/Th17 symptomatic, it is theoretically possible to pass these organisms back and forth if effective treatment is not begun. The less ill a partner is, the easier it will be for them to eliminate the intracellular bacteria with IT.
 
Tissue transplants and blood donations
 
Organs and tissue (Kveim test) from sarcoidosis patients have caused sarcoidosis in the transplanted recipients. This is evidence the Th1/Th17 bacteria can be transferred and triggers the same abnormal immune system response in susceptible people.
 
Sarcoidosis patients are not allowed to give blood by the USA Red Cross but they are allowed to give organ transplants. This report notes that patients who receive a donor organ from a sarcoidosis patients develop the disease, and clean organs transplanted into sarcoidosis patients become infected.
 
Blood banks may not have strict regulations against donations from people with so-called ‘autoimmune’ diseases or Th1/Th17 inflammation but now that the bacterial etiology is known, it is recommended that patients not donate blood, bone marrow, organs or other tissues.
 

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