This is part five in a series covering autoimmune disease. Don’t miss upcoming articles covering environmental medicine and mind body medicine. Check out previous articles covering Loneliness, GI health, nutrition part 1 and nutrition part 2, and hormones.
Autoimmune disease develops when the immune system starts attacking your own tissues. In addition to genetic factors environmental triggers including viruses, bacteria and other infectious agents play a major role in the development of autoimmune diseases. There are several mechanisms behind these triggers that include but are not limited to molecular mimicry, bystander activation and epitope spreading. If you scroll to the bottom of this blog there are some citations that go into great detail about how these mechanisms work if you are interested. In an oversimplified nutshell there can be cases of mistaken identity, our immune system getting overexcited, and chronic inflammation.
What is a chronic infection? All of us are likely familiar with an acute infection: you become briefly ill such as from a cold or the flu and then you recover. Acute infections give our immune system practice. I don’t know about you but it’s now been over 12 months since I’ve had an acute infection (thanks physical distancing!) While this is a nice perk of the pandemic it’s not great for our immune systems. A chronic infection happens when the body can’t seem to muster enough of a defense to adequately resolve the infection. Some examples include hepatitis C and HIV. HIV is treatable but at the time I am writing this there is no way to completely resolve the viral infection. Hepatitis C used to be a lifelong infection but with recent advances in drug therapy it’s now possible to be virus free! Some infections can be latent which means you become ill when initially exposed but then the infectious agent remains in the body dormant only to reactivate at a later time. The classic example is the virus that causes chickenpox will remain latent for decades only to emerge during a time of stress as shingles. Another example of a latent virus is the herpes simplex virus which can cause cold sores or ‘fever blisters’. The herpes family of viruses actually ‘sense’ when stress hormone levels rise and activate to come out of latency. Then the virus triggers a hormone cascade to actually further raise the levels of stress hormones. It’s genius and of course not great for us. There are many pathogens that can be latent or chronic.
When treating autoimmune disease we are always looking for the root cause(s). We can use symptoms as clues that there may be a chronic infection to deal with. Some of those symptoms include; low grade fevers, migratory joint pain, recurrent hives, muscle pain, crawling sensation, as well as exacerbation and remission of symptoms. We can also use the knowledge of which pathogens are commonly associated with particular autoimmune diseases. For example, the bacteria klebsiella is implicated in the development of ankylosing spondylitis (AS), an autoimmune joint disease impacting the spine. Antibodies against klebsiella are found in AS patients. AS patients tend to have elevated levels of klebsiella in their stool and reduction of this bacteria can reduce the severity of AS. A combination of signs, symptoms and empirical knowledge will lead us to suspect chronic infections.
Unfortunately, testing for chronic infections is challenging. Sometimes standard lab work can provide clues. We can see chronically low or high white blood cells and/or a chronically low/low normal RDW on a CBC. When testing for specific infections we must look for antibodies specific to that infection. This requires running several tests for each infection you are looking for. Let’s use Epstein-Bar (EBV) as an example. When looking for this infection we will often run: EBV viral capsid IgM, EBV viral capsid IgG, EBV nuclear antigen, and EBV early antigen IgG. If we want to test for other viral infections we will need a similar list of labs. You can see the list of labs gets very long and it can become incredibly expensive.
Once I suspect a chronic infection the first steps I take are to support the person as a whole. All of us are exposed to infectious agents that can cause chronic infections. Instead of jumping to herbs/medications that can eradicate the infection I first want to identify what about this patient is allowing this infection to persist. In Naturopathic medicine we use the language ‘terrain’ to describe the environment in the host (patient). We need to make the terrain more inhospitable, strengthen the patient, and then go after the infection.
The following are some avenues we explore together in strengthening the patient and creating an inhospitable terrain:
- Getting blood sugar in check
- Optimize nutrition
- Making sure stressors and more importantly the stress response is under control
- Prioritizing rest
- Ensuring adequate sleep
- Optimize GI health and the microbiome
I will leave you with an example from Hashimoto’s disease, a condition I treat frequently. People with Hashimoto’s Thyroiditis (HT) have higher levels of EBV viral capsid IgG and early antigen IgG. In one study researchers looked at surgical specimens of thyroid tissue and found that 34.5% of the tissue from HT patients contained signs of EBV etiology. Does this mean that I test every Hashimoto’s patient for EBV during the first visit? No. We start with the list above while monitoring thyroid function and antibodies. Remember it’s not about the bug, we must work on the ‘terrain’ first and then go after chronic infections.
References:
Infectious diseases and autoimmunity
Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease
Virus infection, antiviral immunity, and autoimmunity
Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1 and Part 2
Social stress and the reactivation of latent herpes simplex virus type 1
The relationship between Klebsiella infection and ankylosing spondylitis
Study of Epstein–Barr virus serological profile in Egyptian patients with Hashimoto’s thyroiditis: A case-control study
The role of Epstein-Barr virus infection in the development of autoimmune thyroid diseases