Rheumatic fever was a disease which was common in America, Europe and in most countries of the world in the past, but in countries which have gone through modernization due to the institution of scientific advancements (which lead to the industrial revolution, for instance)the frequency of the disease has become so low, and the seriousness of the disease has become so mild, that current physicians have little knowledge concerning it as a disease entity and would have difficulty in identifying a high-grade case even if it was presented to them.
Recently, in 1997, Benedict Massell, MD, a physician experienced in treating rheumatic fever in times past, and who knows the seriousness of the disease, wrote a book: “Rheumatic Fever and Streptococcal Diseases” and it was published by Harvard Press. Gene Stollerman is another physician who had experience treating rheumatic fever and he wrote an electronic article: “Rheumatic Fever As We Enter the 21st Century”. It it he gives dire warnings about ignoring rheumatic fever as a disease process. There has never been a vaccine for it, for instance, and it could return with a vengeance. George Veasey, et.al. in 1987 published a paper which indicated that rheumatic fever cases had started to increase in frequency in the Rocky Mountain area of the USA during the early to mid 1980’s. Statistics indicate that more young people, under thirty years of age, died of rheumatic fever in 1965, than any other infectious disease. Statistics indicate that there were over 100,000 cases of rheumatic fever and one million cases of streptococcal infection in the Navy during WW II. To think that it disappeared is foolhardy. To think that the severity of rheumatic fever became less so that it is poorly recognized is not foolhardy. It is true. Like any disease, rheumatic fever can appear as a subtle case or as a high grade case wherein it can cause a person’s death in days.
I worked as a general practitioner for over thirty years, first in the Navy and then for 23 years in Washington State. I practiced in a small semi-rural town with no modern industries and a great amount of economic privation. Eventually, I had three clinics with the main one in Toledo, Washington and one in each of the neighboring small towns of Winlock and Onalaska. I had physician assistants helping me see patients. In the rural area where I practiced there were mainly logging, millwork, and construction jobs.
Over the years, I had many, many patients who had lumbar/buttock pain and limb neuropathy and shoulder/cervical pain and arm neruopathy. Often patients had spinal surgery and didn’t get better. I thought back on my experience about six years ago and I could not remember any patient getting better after spinal surgery in a reasonable length of time. Some people got better after months or years, but that didn’t mean the surgery helped. Also, some people improved with manipulation after months or years and some people got better one their own. Some people didn’t get better no matter what treatment was given them.
With the above in mind I also knew the diagnosis of fibromyalgia had increased during the previous ten years and it was an idiopathic disease, that is with no known cause,that caused chronic pain, usually about the shoulder and hip girdle, but it often featured fatigue,and the mental components of depression and anxiety, along with it also. I knew that pain was one of the prime indications of inflammation. All physicians learned that dolar, rubor, tumor, and calor (pain, redness, swelling, and heat)are the principle signs of inflammation. Usually pain, or dolor, is the most common symptom patients experience since the others may be very subtle or if the problem is internal, there is no way to observe the other three signs. Naturally, if a person sustained an acute injury such as a sprain, fracture or laceration, they would experience pain from that assault, but my patients had chronic pain and no continuous physical assault that I could observe. I did realize, over time, that they were experiencing a subtle chronic assault to very sensitive structures, however: peripheral nerves. I also realized that inflammation was involved because a long lasting steroid anti-inflammatory injection would give many patients some relief for a number of days or a few weeks.
Since my patients were experiencing chronic neurological pain that would improve temporarily by treating them with steroid antiinflammatory medications, I decided they must have an inflammatory disease and it was made worse by trauma, like a fall, lifting something, repetitious lifting, or a twist. Often the trauma was mild. Severe trauma would bring on a more painful syndrome, commonly.
I determined by physical examination and an analytic neurological examination that the patient’s problems were in the distal brachial plexus and the distal sacral plexus not in the spine, but they did have radiating pain to the spine. That is the reason spinal surgery did not help them at all. I did not know the cause of the inflammation and why it was localized, but I did know that the narrow passageways through which the neurovascular bundles passed, deep in the pelvis to the buttock (the greater sciatic foramen) and deep within the shoulder(the axillary canal)had something to do with it. I realized that the large nerves, the association of a dense vascular network within the nerves, the tight passageways, and the high-grade motion of the hip and shoulder were connected to the development of inflammation and then the chronic neurological pain.
I attracted 700 miserable, painful, patients. Many of them had had surgery to the lumbar or cervical spine, often many surgeries, with no great results. I learned that they had many dermatological signs in common. They all had some kind of rheumatoid disease, I learned that many had had cancer and arteriosclerotic diseases. Eventually I realized that they all had severe dermographism and palmar and plantar erythema. Dermographism is a phenomenon that appears when the skin is firmly scraped wherein a erythematous (reddish) streak appears. My group of patients had severe inflammatory responses and in some patients a urticarial, or hive-like structure would appear and it would remain for a long period. I realized that red palms and the bottoms of feet were caused by chronic trauma as patients handled objects and as they weight-bore while walking. Now, I realized that the complex neurovascular bundles containing the sciatic nerve that innervated the lower extremity and the perineal nerve that innervated the vulva in the female and the scrotum and penis in the male were both affected. I determined that the brachial plexus which gave rise to the nerves of the arm, upper chest, and upper back were being inflamed by the abrasion and compression which took place with motion, repetitious at times and perhaps a flail limb injury.
In the literature I noted a neuroapthy was described, which was autoimmune in nature (Mayo Clinic Peripheral Nerve Group (Dyck, et al) and Weill Medical College, (Latov). I realized that the rheumatic diseases were autoimmune, systemic diseases. I realized that the chapter in “Harrison’s Principles of Internal Medicine” concerning rheumatoid arthritis indicated that it was an autoimmune, systemic disease, the cause was not known, but at times patients seemed to have a mild sickness sometime before a flare developed. Patients experienced neuropathies and often the neuropathy was the only indication of the disease, and there were even internal organ infarctions. I realized that that one paragraph held information which was important in this painful malady, which my patients experienced. I did not know the cause though, so I continued my epidemiological clinical study as I examined my patients repetitiously.
Eventually I had a break-through! A new patient came in and she had been diagnosed with fibromyalgia when she lived in Texas(this syndrome is caused when all the sensory nerves in the shoulder girdles and the hip girdles are involved simultaneously). She had the same dermatological features (petechiae, telangectasias, spider nevi) on her cheeks and “v” of the neck whereon sun light could strike her most meaningfully. She had angiomas (small round red marks) on her abdomen, chest and proximal arms and legs. She had many nevi (moles)and some seborrheic keratosis (age marks) even though she was only thirty-four years old. I saw her five times and always asked her questions and examined her in an effort to find out why she and the other 700 patients had neurological pain. About the last time I saw her I asked her when the dermatological features first arrived. She indicated that they developed after she had had rheumatic fever six years before.
I was incredulous because I had been taught that rheumatic fever was not present in developed countries and hadn’t been a problem in the USA since the 1960’s or so. I reviewed the disease in the the “Merck Manual” and “Harrison’s Principles of Internal Medicine” and then asked her about the details of her acute disease episode. Her signs and symptoms matched the text perfectly. I tested her serologically and she was positive ASO titer and Anti-DNAse B titer). I then tested many of my other patients and they were also highly positive. Many of my older patients knew they had had scarlet or rheumatic fever in the distant past and I learned they are basically the same disease. Other patients had had a severe case of chicken pox, mono, measles, or even the worst flu they had ever had and the cursory diagnoses made at the time of their sicknesses were incorrect. Other patients had had been diagnosed to have had viral meningitis. I realized that there were erroneous diagnoses made previously, often by parents. Sometimes people had multiple cases of chicken pox, but it was really rheumatic fever. I realized I had diagnosed some of my patients improperly too, in the past and didn’t realize the potential ramifications of the disease in a thorough fashion.
I studied the disease, rheumatic fever, thoroughly. I realized it was an autoimmune disease due to a common organism: Streptococcus pyogenes (strep A). All the medical books specified that it was a high grade disease and certain criteria were used to diagnose it: the Jones criteria developed during WW II when there were 100,000 cases in the US Navy. I learned that Veasey discovered an area with more frequent cases of clinical rheumatic fever in the Salt Lake City (Rocky Mountain) area and published a paper in 1987. I learned that it is endemic in much of the world and it could be “jet propelled” into more modern societies quickly and easily (Gene Stollerman, MD). I learned of a very good text by Benedict F Massell, MD written in 1997: “Rheumatic Fever and Streptococcal Infections”. I found four older sites in the literature wherein rheumatic fever was linked to the development of arteriosclerosis, especially coronary artery disease. I determined that coronary artery disease, pericarditis, cardiac valve disease, left ventricular hypertrophy, idiopathic cardiomyopathy, and cardiac arrhythmias were all caused by the autoimmune response to Streptococcal pyogenes infections through a person’s lifetime.
I realized that many of my patients had rheumatic fever in a subtle way, a sub-clinical way, with just a feeling of fatigue, an occasional chill, dizzy feeling, more aches and pains, or just not feeling up to par. I found that description, eventually, in a medical text written when rheumatic fever was common in a high-grade way in America as well as other modern countries: “Osler’s Principles and Practice of Medicine” published in 1935. Dr. Osler was the most famous physician, perhaps, of his era.
Now I knew the whole story: the back pain, upper and lower, and limb neuropathies were caused by autoimmune response to a common germ: Streptococcus pyogenes also called Strep A. I realized from reading information in Russian sources that it tended to be familial and caused what was termed: familial rheumatism. I read in much older sources that rheumatic fever was called acute rheumatism and all the miserable problems thereafter were called chronic rheumatism. I learned that early American doctors called sciatica: sciatic rheumatism. I realized that the division of medicine into specialties, compartmentalized medical science artificially, so that modern doctors did not have a chance to continue the diagnostic progress which was being made in the late 1800’s and early 1900’s.
I have recorded the cause of cancer in another article on this venue. It is caused by the same underlying autoimmune disease, but the physical and physiological environment in certain tissues causes cancer to develop in those tissues and organs more than others, but it too is a systemic disease and it is part of the rheumatism concept.
As I mentioned above, I eventually attracted 700 miserable painful patients and they all had painful neuropathic pain. The clinical presentations were: brachial plexus neuritis, lumbosacral plexus neuritis, femoral neuritis, median neuritis, ulnar neuritis, and pudendal neuritis. These large nerves are easy to isolate on an analytic neurological examination. They all pass through tight passageways and with body movement at the shoulder, hip, elboe and wrist vascular inflammation within the nerves themselves becomes more severe via the “triple response of Lewis” phenomenon. For the above reason surgery for carpal tunnel syndrome, ulnar neuropathy, low back pain and cerival pain are usually unsuccesful. Since the neurological pain is exacerbated or brought on by an accident or a repetitious activity the local manifestations of the systemic autoimmune disease appears to be connected to work activities and so workers’compensations claims are made and they are the most common type of claim in the State of Washington. Statistical information indicate that at least 80% of people have low back pain and sciatica, at least mildly in their lives and that is an indicaton how common rheumatoid autoimmune vasculitis is in our society. It is more common in more primative societies.
Since rheumatic fever is a chronic, autoimmune, inflammatory “systemic disease” there are many subtle and not so subtle ramifications. A good way to think about it is that each tissue and each organ responds in its own idiosyncratic way to the inflammatory, autoimmune assault. Many of the clinical presentations have been given different names. Two of them are: Kawasaki’s disease and Guillain-Barre’ syndrome. Often, there are mistaken diagnosis because rheumatic fever often has a rash. The rash can be variable and can look like chicken pox, measles, mononucleosis, hives, or heat rash, but it is important to realize that the rash can have a variable appearance. Patients can have rheumatic fever and not have a rash at all! Often the disease is diagnosed as viral meningitis, due to its cerebral component, or influenza (the flu). Symptoms of respiratory disease, abdominal cramping and pain, diarrhea, fever, mental changes (sleeiness or delirium), photophobia, and body pain should alert a person that rheumatic fever is a good possibility. If children have growing pains in the legs it is a sign of autoimmune inflammation of the growing points of the legs (epiphysis). Juvenile arthritis and the adult rheumatic diseases (connective tissue diseases) are all caused by this underlying autoimmune disease process.
Since, as I mentioned above, rheumatic fever is a systemic autoimmune disease and that it is ofen chronic or semi-chronic in nature, each organ and tissue is affected in its own way. The heart features autonomic neuropathy, which causes cardiac arrythmias, the heart contracts on itself and so via the “triple response of Lewis” phenomenon there is increased inflamation of the capillaries, arterioles, venules and lymph vessels of the heart and patients suffer changes within their myocardiums (heart muscles). The result is LVH or enlargement of the left ventricle since it is contracting more firmly than the rest of the heart and in more severe cases patients develop an enlargement of the total heart with total heart malfunction. This condition is termed idiopathic cardiomyopathy and it leads to total heart failure and at times cardiac transplant procedures. It is recognized commonly that the cardiac valves will become inflammed and calcificed from rheumatic fever. To have such chronic changes, however, a person must have had low grade rheumatic fever for many, many months or years of their lifetimes. In James Osler’s famous medical book, “Osler’s Principles and Practices of Medicine, Twelfth Edition”(Appleton-Century, 1935), he mentions that rheumatic fever can exist in variable forms including the vary subtle form wherein a patient may just not feel “up to par”. Think about how such subtle symptoms are usually ignored by patients and medical practitioners. Think about what physicians and patients are missing. Think what simple WW II penicillin can do for those who have mild sicknesses, which patients just ignore or which doctors just dismiss as a viral disease with no proof.
Other cardiac problems are: pericarditis and coronary artery disease. The reason the former exists is that the inside of the pericardial membrane abrads against the epicardium, the outside of the heart muscle, and the friction, which takes place while the heart is beating causes and increased “triple response of Lewis” phenomenon, which is an inflammatory condition. In the medical text by Harrison, mentioned above, it stipulates that over 50% of patients with rheumatoid arthritis have pericarditis on autopsy. Why?, it is caused by the same disease process! Coronary artery disease develops due to the same compression and abrassion since they are located ourside the myocardium (the heart muscle). The pericardial membrane compresses and abrades the cardiac vasculature during the compressive function of the heart and so more inflammation is developed in those arteries than other in the body and so myocardial infactions (obstructive heart attacks) are common in society. Most people who have myocardial infarctions have some somatic rheumatoid arthritis and have experineced neuropathy, especially sciatic neuropathy or simple low back pain. The syndrome of sudden ischemic cardiac death, or SICD, is that malady wherein a relatively young person dies suddenly. The patients usually have some coronary arteriosclerosis and some LVH (left ventricular hypertrophy or enlargement). The patients, however, die from a cardiac arrhythmia that develops spontaneously due to rheumatic autoimmune autonomic neuropathy, that is an abnormality to the nerves controlling the heart caused by the inflammatory vasculitis which is the basic lesion of rhumatoid, autoimmune disease.
Other important diseases, which are really just target-organ manifestations of rheumatoid disease, are caused by the underlying disease of rheumatoid autoimmune vasculitis: cancer of all kinds, endocrine diseases including Addison’s disease, Cushings syndrome, diabetes, hypothyroidism, polycystic ovary disease, testicular failure, various pituitary abnormalities, parathyroid conditions, etc. Since somatic mutations can occur that cause tumors, the microadenomas of the pituitary,adrenal glands, and other endocrine glands are faily common.
One may say, with certain restrictions, that most of the non-infectious diseases, that fill todays medical books, are caused by this systemic, inflammatory, autoimmune disease process. Since Streptococcus pyogenes is a common microorganism and since it is ubiquitous to the human population of the world and other vertebrates it is a true bilateral zooinosis. Naturally, the control of this disease process needs to be done world-wide. To help bring more attention to this disease process I am writing a book titled, “Rheumatism Enigma Unraveled” and it will be available from typical outlets in a few months.
I suppose the above information is not absolutely true, but it is I am sure, well over 95% true. When other medical scientists take interest and test this theory it will become a more trusted concept and many of the diseases with which patients and physicians struggle with, diaily will be abled to be treated by autoantigen blocking agents and prevented with a vaccine, both of which will have to be developed.
