Rheumatism by Dr. Lance Christiansen: Difference between revisions
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The following information concerning the chronic, systemic, inflammatory disease of rheumatism was obtained from reading a great number of texts and journal articles during my education in biology, during two years of premedical studies, and during five years of formal medical education. In addition, I referred to texts and medical journals, daily, during a 28 year career as a general practitioner in medicine, and especially during the last eight years during which time I conducted a clinical, academic and epidemiological investigation in an effort to determine the cause of, and hopefully a treatment for, painful, chronic, neuropathic pain. Eventually I learned, as Niels Bohr had learned concerning the unknown issues intrinsically associated with the discovery of atomic fission: "Every great and deep difficulty bears in itself its own solution." Although information I had | The following information concerning the chronic, systemic, inflammatory disease of rheumatism was obtained from reading a great number of texts and journal articles during my education in biology, during two years of premedical studies, and during five years of formal medical education. In addition, I referred to texts and medical journals, daily, during a 28 year career as a general practitioner in medicine, and especially during the last eight years during which time I conducted a clinical, academic and epidemiological investigation in an effort to determine the cause of, and hopefully a treatment for, painful, chronic, neuropathic pain. Eventually I learned, as Niels Bohr had learned concerning the unknown issues intrinsically associated with the discovery of atomic fission, as written in the text, "The Making of the Atomic Bomb" (Richard Rhodes, Touchstone, 1986): "Every great and deep difficulty bears in itself its own solution." Although information I had accumulated through my education and during my daily work as a physician contributed, in general to my medical knowledge, most of the salient information, which permitted me to "break the code of rheumatism", the underlying autoimmune disease, which causes a multitude of "target-organ manifestations", including most cases of chronic neuropathic pain and other neurological signs and symptoms, was gained through "repetitiously" interviewing patients concerning their, and their family members', medical histories and "repetitiously" conducting analytic, neurological, physical examinations on each of the 700 patients, who had chronic neurological pain, who had referred themselves to my clinic. After I was quite sure that I had identified the heretofore undiscovered "infectious cause of autoimmunity" I conducted certain specific antibody tests on the serum of over one hundred patients, of the 700 patients, at random, who experienced severe, chronic neuropathic pain and 70 of the 102 individuals' serum had positive tests. The patients' medical histories, their family medical histories, the signs and symptoms of recurrent infections, and the serum antibody tests, together, assured me, to a great degree, that I had managed to determine the cause of their medical problems | ||
Of the twenty-eight years that I practiced general medicine I owned my own clinic for twenty-one of the years. I examined and treated patients during, approximately, | Of the twenty-eight years that I practiced general medicine I owned my own clinic for twenty-one of the years, which provided an environment that enabled me to work and think somewhat independently. I examined and treated patients during, approximately, 220,000 office visits, after-hours urgent care visits, and I accomplished at least 2000 house calls. Regularly, I treated males and females, of all ages, for all diseases, the latter, of course, up to my ability. At times, I treated family members for up to four generations. The continuity of medical care that I provided, in a semi-rural setting, enabled me to learn a great amount of medical information not written in typical medical texts. In addition, my clinic was located in an economically depressed area of S.W. Washington State and, over time, I learned that poorer people are often sicker people! | ||
Over the years I had treated many patients who experienced lumbosacral/buttock (sciatic) and shoulder/cervical pain, with neuropathic signs and symptoms into the appropriate limb, which was often severe and chronic | Over the years I had treated many patients who experienced lumbosacral/buttock (sciatic) and shoulder/cervical pain, with neuropathic signs and symptoms into the appropriate limb, which was often severe and chronic. The adverse condition affected younger persons, even teenagers, but older people, over sixty years of age, were also frequent victims. Usually such pain was thought to be caused by the compression of spinal nerves by herniated spinal-discs. | ||
Many, many patients, through the years, had failed to experience an improvement in the above described painful malady even if they underwent spinal surgery, often, many spinal surgeries. Usually, I was treated about twenty-five patients who had experienced the failure of lumbar and cervical spinal surgery to decrease their painful symptoms. During the winter of 2002, two more patients, in their forties, failed to experience a decrease in neurological symptoms and signs after undergoing lumbar spinal surgery and that experience, which saddened the patients and made me very disappointed, stimulated me to initiating a clinical investigation to see if I could determine that another cause could be determined for my patients' lumbosacral/buttock and shoulder/cervical neurological pain. I thought there was something "rotten going on" within the various professional aspects of "spinal care", in general, and spinal surgery, in particular. That experience, and the intellectual study that it stimulated, led to an epidemiological study wherein I traveled to eighteen countries and spoke with physicians in many locals, but more importantly, with people "on the street". | |||
Rheumatism is considered an archaic term in medicine for it is not listed as a subject in most, modern, medical texts. For instance it is not listed as a subject in the text, ''Harrison's Principles of Internal Medicine, 16th Edition'' (Kasper,D., McGraw-Hill, 2005). | Rheumatism is considered an archaic term in medicine for it is not listed as a subject in most, modern, medical texts. For instance it is not listed as a subject in the text, ''Harrison's Principles of Internal Medicine, 16th Edition'' (Kasper,D., McGraw-Hill, 2005). | ||
Revision as of 17:35, 12 January 2012
| Rheumatism by Dr. Lance Christiansen | |
| ICD-10 | M79.0 |
|---|---|
| ICD-9 | 729.0 |
| MeSH | D012216 |
Editor-in-Chief: Lance Christiansen, D.O.
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Overview
The following information concerning the chronic, systemic, inflammatory disease of rheumatism was obtained from reading a great number of texts and journal articles during my education in biology, during two years of premedical studies, and during five years of formal medical education. In addition, I referred to texts and medical journals, daily, during a 28 year career as a general practitioner in medicine, and especially during the last eight years during which time I conducted a clinical, academic and epidemiological investigation in an effort to determine the cause of, and hopefully a treatment for, painful, chronic, neuropathic pain. Eventually I learned, as Niels Bohr had learned concerning the unknown issues intrinsically associated with the discovery of atomic fission, as written in the text, "The Making of the Atomic Bomb" (Richard Rhodes, Touchstone, 1986): "Every great and deep difficulty bears in itself its own solution." Although information I had accumulated through my education and during my daily work as a physician contributed, in general to my medical knowledge, most of the salient information, which permitted me to "break the code of rheumatism", the underlying autoimmune disease, which causes a multitude of "target-organ manifestations", including most cases of chronic neuropathic pain and other neurological signs and symptoms, was gained through "repetitiously" interviewing patients concerning their, and their family members', medical histories and "repetitiously" conducting analytic, neurological, physical examinations on each of the 700 patients, who had chronic neurological pain, who had referred themselves to my clinic. After I was quite sure that I had identified the heretofore undiscovered "infectious cause of autoimmunity" I conducted certain specific antibody tests on the serum of over one hundred patients, of the 700 patients, at random, who experienced severe, chronic neuropathic pain and 70 of the 102 individuals' serum had positive tests. The patients' medical histories, their family medical histories, the signs and symptoms of recurrent infections, and the serum antibody tests, together, assured me, to a great degree, that I had managed to determine the cause of their medical problems
Of the twenty-eight years that I practiced general medicine I owned my own clinic for twenty-one of the years, which provided an environment that enabled me to work and think somewhat independently. I examined and treated patients during, approximately, 220,000 office visits, after-hours urgent care visits, and I accomplished at least 2000 house calls. Regularly, I treated males and females, of all ages, for all diseases, the latter, of course, up to my ability. At times, I treated family members for up to four generations. The continuity of medical care that I provided, in a semi-rural setting, enabled me to learn a great amount of medical information not written in typical medical texts. In addition, my clinic was located in an economically depressed area of S.W. Washington State and, over time, I learned that poorer people are often sicker people!
Over the years I had treated many patients who experienced lumbosacral/buttock (sciatic) and shoulder/cervical pain, with neuropathic signs and symptoms into the appropriate limb, which was often severe and chronic. The adverse condition affected younger persons, even teenagers, but older people, over sixty years of age, were also frequent victims. Usually such pain was thought to be caused by the compression of spinal nerves by herniated spinal-discs.
Many, many patients, through the years, had failed to experience an improvement in the above described painful malady even if they underwent spinal surgery, often, many spinal surgeries. Usually, I was treated about twenty-five patients who had experienced the failure of lumbar and cervical spinal surgery to decrease their painful symptoms. During the winter of 2002, two more patients, in their forties, failed to experience a decrease in neurological symptoms and signs after undergoing lumbar spinal surgery and that experience, which saddened the patients and made me very disappointed, stimulated me to initiating a clinical investigation to see if I could determine that another cause could be determined for my patients' lumbosacral/buttock and shoulder/cervical neurological pain. I thought there was something "rotten going on" within the various professional aspects of "spinal care", in general, and spinal surgery, in particular. That experience, and the intellectual study that it stimulated, led to an epidemiological study wherein I traveled to eighteen countries and spoke with physicians in many locals, but more importantly, with people "on the street".
Rheumatism is considered an archaic term in medicine for it is not listed as a subject in most, modern, medical texts. For instance it is not listed as a subject in the text, Harrison's Principles of Internal Medicine, 16th Edition (Kasper,D., McGraw-Hill, 2005).
Within the 12th editon of the same text, published in 1991, the only listing for rheumatism is psychogenic rheumatism and part of the short paragraph explaining it is as follows, "PSYCHOGENIC RHEUMATISM Patients may experience severe joint pain involving a few to several joints without physical findings of arthritis. These patients are often convinced that they have rheumatoid arthritis, systemic lupus erythematosis, or another rheumatic connective tissue disease. This disorder is recognized by the inconsistencies, exaggerations, and emotional lability of the patient during the history and physical examination..." I think that the above synopsis makes obvious the author's lack of observation skills, the author's lack of patient concern, and it is an arch-type example of how some physicians find fault with patients when the physician does not know "what is going on". In addition, physicians who have the above nature seem not to be able to say to a patient, "I don't know".
From, at least, the late 1700's until the early 1900's the terms rheumatism and rheumatic fever were used, at times, in an interchangeable fashion as noted within the chapter "Medicine" and the paragraph, "of the Rheumatism" within the first edition of the "Encyclopedia Britannica" (By a Society of Gentlemen in Scotland, In Three Volumes, Printed for A. Bell and C Macfarquhar, and fold by Colin Macfarquhar, at his Printing-office, Nicolson-street, Edinburgh, M.DCC.LXXI.) As time passed by the terms, "acute rheumatism" and "inflammatory rheumatism" were terms frequently used to describe episodes of acute rheumatic fever. One might think that the term rheumatic fever described a disease, at times with a high fever, which was rheumatic in character since other symptoms and signs of the disease were known to be part of the rheumatism concept (migratory arthritis, back pain or lumbago, gastrointestinal abnormalities, cardiac problems, delirium, coma, seizures, etc.). It was known in the late 1700's, as quoted in the first edition of the Encyclopedia Britannica, mentioned above, that: "The chronic rheumatism is either the remains of a rheumatic fever, or a continuations of pains that proceeded at first from lesser but neglected colds." The information within that quote indicates that authors of the day, in the late 1700's, knew that acute rheumatism (rheumatic fever) could cause chronic rheumatism, but also they knew that less severe episodes of respiratory disease, "...lesser but neglected colds.", could also cause chronic rheumatism.
Contagions, or diseases that travele through affected populations, were known to exist since before the time of Hippocrates. Their cause was a mystery and though physicians of the Hippocratic persuasion, distanced themselves from medical dogma and treatments, which were championed by certain practitioners..."who pretend to be very pious and particularly wise..."It is my opinion that those who first call this disease 'sacred', were the sort of people we now call witch doctors, faith healers, quacks, and charlatans." ("Hippocratic Writings, G.E.R. Lloyd, Editor, Penguin Books, 1983) Other sources indicate that sick individuals were thought to be "under the influence", which was... "a quality supposed to flow from the heavenly bodies, either with their light or heat; to which astologers idly ascribe all sublunary events." (Encylopedia Britannica, 1st Edition, cited above). At times the word influenza referred to the effects, salutary or adverse, that God or gods could affect on an individual or a population. In fact the word, influenza is derived from the Latin, and thereafter Italian, for "under the influence" and in the case where many people in a locality suddenly became similarly sick they were thought to be under the influence of the heavens or the gods (or God.
The tobacco mosaic virus was the first virus discovered in 1892 by Iwanoski in Russia and in 1899 by Beijerinck in Holland ("Microbiology, Second Edition" (Davis, et al., Harper and Row Publishers, 1973) Shortly thereafter a virus was determined to be the cause of yellow fever by the use of Koch's Postulates. Epidemiological observation had been accomplished earlier by the Cuban physician Carlos FIndlay and he documented, thoroughly, why he thought the mosquito spread the agent of yellow fever disease. The discovery of the cause of yellow fever, which was a great breakthrough in medicine, caused physicians to think that viruses would likely be the cause of other infectious disease processes. Since electron microscopy was not invented until the 1930's, however, the nature of viruses could not be studied with great detail. Within the text, "Microbiology, Second Edition", cited above, the authors indicate: "For the first third of this century viruses could be detected only by their pathogenic effects on living hosts, and progress was slow." Virus seemed an appropriate word for the cause of the pandemic that coincided with the 1st World War since its meaning in Latin is, poison.
In modern times the word influenza, and its "slang", "the flu" usually describes a disease with certain symptoms and signs: a respiratory disease, gastrointestinal signs and symptoms, at times, lethargy, sleepiness, headache, at times, weakness, and body pain. It is generally thought to be caused by a certain virus, but in most individual cases a specific viral cause is never proven via the use of Koch's Postulates or even by testing for a rise in a specific viral antibody titer with the use of acute and convalescent serum samples. Therefore, the use of the words "flu" or "influenza" are clinical "catch alls", and in most instances they are inexact terms. If a patient is professionally diagnosed with "the flu" the clinician, therefore, is simply making an "empiric guess". Sir William Osler, in his text, "Osler's Principles and Practice of Medicine, Twelfth Edition" (Sir William Osler and Thomas McCrea, D. Appleton-Century Company, 1935) comments about influenza: "The term "influenza" is often used loosely and applied to acute upper respiratory tract infections, acute febrile illnesses of various kinds and even to digestive tract disturbances. It is often used as a term to fit an illness without any proof of its correctness." Surprisingly, the signs and symptoms of "the flu" are similar to subacute rheumatic fever.
I hypothesize that applying the name "the flu" to a disease state, usually, probably 99.9% of the time, has no relation to the etiology of a patient's disease state, or the pathophysiology of their subjective and objective findings, some of which are mentioned in the above paragraph. Even if a physician, or other medical professional, claims that a patient has "the flu" it is likely that it is a wrong diagnosis. To assure that such a diagnosis is accurate, acute and convalescent serum testing to determine if there is a rise in a specific antibody, or group of antibodies, must be accomplished to assure that the certain, suspected microorganism surely caused the disease in question. If such a test is not accomplished the diagnostic assessment provided is a "guess".
In older texts such as Osler's Principles and Practice of Medicine, Eighth Edition (McCrea, T., Appleton-Century Co., 1912), the following is mentioned about rheumatism in the section concerning acute chorea. Chorea is defined as, "the ceaseless occurrence of a wide variety of rapid, highly complex, jerky movements that appear to be well coordinated buy are performed involuntarily...Sydenhams c., an acute , usually self-limited disorder of early life, usually between the ages of five and fifteen, or during pregnancy, and closely linked with rheumatic fever." (Dorland's Illustrated Medical Dictionary, 27th Edition, W.B. Saunders Co., 1985) "Rheumatism.--A causual relationship between rheumatism and chorea has been claimed by many since the time of Bright. The English and French writers maintain the closeness of this connection; on the other hand, German authors as a rule, regard the connection as by no means very close. Of the 554 cases, in 15.5 per cent., there was a history of rheumatism in the family. In 88 cases, 15.8 per cent., there was a history of articular swelling, acute or subacute. In 33 cases there were pains, sometimes described as rheumatic, in various parts, but not associated with joint trouble, the percentage is raised to 21. It is rather remarkable that in our Baltimore series the percentage with a history of rheumatim was the same, 21.6...with the exception of rheumatic fever, there is no intimate relationship between chorea and the acute diseases of childhood...With no disease, not excepting rheumatism, is it so constantly associated. I collected from the literature the records of 73 autopsies; there were 62 with endocarditis. The endocarditis is usually of the simple variety, but the ulcerative form has occassionally been described...pericarditis is an occasional complication of chorea, usually in cases with well-marked rheumatism." ("Osler's Principles and Practice of Medicine, Eighth Edition", cited above)
By 1935, when the 12th Edition of Osler's text was published the use, and meanings, of the terms rheumatism and rheumatic fever experienced a segregation and "rheumatism" is not listed in its index. Rheumatic fever, however, is described quite thoroughly (compared to modern texts) since a great amount of clinical knowledge about rheumatic fever, as an acute, a subacute, and less than subacute disease process had been developed. The knowledge that rheumatic fever was caused by Streptococcus pyogenes, a fact discovered by both Alvin Coburn in the USA and Wilfred Collis in England in 1931, was not, however, included in the text, which is an indication of the time it takes for physicians, even highly experienced physicians, to accept new ideas even if they are well proven. The concept of chronic rheumatism still existed, but it was diminishing in the minds of physicians, and medical authors, because, in my opinion, the specialty divisions of medicine, which had been experiencing accelerated development for over a decade, decreased the conceptual understanding of systemic disease processes. Medicine as an art and science was being coerced into following the specialty paradigm wherein disease concepts had to be fit into the various specialty divisions that were being developed. Thus, a systemic disease concept, such as rheumatism, slowly disappeared from the minds of physicians even though many diseases were, and are, known to be systemic in nature. For instance, within "Webster's Encyclopedic Unabridged Dictionary of the English Language" (Random House, 1989) the following definition for rheumatoid arthritis is provided: "rheumatoid arthritis,...a chronic disease marked by signs and symptoms of inflammation of the joints, frequently accompanied by marked deformities, and ordinarily associated with manifestations of a general, or systemic, affliction."
Dictionaries, in general, and "Dorland's illistrated Medical Dictionary, 27th Edition", cited above, in particular, tend to preserve the historical meaning, and often the philological evolution, of words, so the word rheumatism is profusely defined. I will select certain aspects of the definition from the above text: "Any variety of disorders marked by inflammation, degeneration, or metabolic derangement of the connective tissue structures of the body, especially the joints and related structures, including muscles, bursae, tendons and fibrous tissue...Rheumatism confined to the joints is arthritis. articular r., 'acute r, rheumatic fever..."cerebral r"., acute rheumatic fever marked by chorea, delirium, convulsions, and coma..."r. of the heart", involvement of the heart by trhe rheumatic fever process."Inflammatory r"., rheumatic fever..."lumbar r"., lumbago..."muscular r"., fibrositis..."subacute r"., a mild but protracted form of rheumatism." Since connective tissue, fibrous tissue, are parts of all organs, the skin, bones, tendons, ligaments, muscles, the heart, kidneys, gastrointestinal organs, the brain, etc., a disease that affects such tissue adversely will be, naturally, systemic in nature.
Hippocrates, or physicians of the Hippocratic persuasion, recorded within the book, The Sacred Disease, published within the text, "Hippocratic Writings", cited above, many case histories, which, in sum, indicate that the patients discussed, who became sick in an epidemic, experienced rheumatic fever. During the second century AD Claudius Galenus, commonly termed, simply, Galen was the first individual known to have coined the word rheumatism (rheumatismos). In the text, "Rheumatic Fever and Streptococcal Infection" (Massell, M., Harvard Press, 1997) the author provides a historical study of rheumatic fever. Guillaume Baillou (1538-1616) in France, during the Renaissance, wrote clearly about rheumatic fever. Later, Thomas Sydenham, during the mid 1600's, differentiated scarlet fever from measles and described rheumatic fever. Even though a great amount of clinical knowledge was gained about rheumatic fever its cause puzzled physicians, and other investigators, for hundreds of years for it wasn't understood that its cause was Streptococcus pyogenes until 1931. "In 1885,...Dr. Alfred Mantle presented a paper on infectious sore throat before the Section on Public Medicine at the annual meeting of the British Medical Association...He concluded that rheumatism was a common complication of infectious sore throat..." Further, "Because of its joint manifestations, rheumatic fever is included by the American Rheumatism Association as one of more than eighty different rheumatic conditions that it classifies." In addition, "Guillaume Baillou (1538-1616,...a Parisian physician apparently was the first to use the term "rheumatism" (rheumatismos) for polyarthritis..." "On the other hand the method by which this affection attacks which is falsely called catarrh; (for the name catarrh signifies distillation from the head) it seems better to speak of the others as rheumatism..." Dr. Baillou goes on to provide a very good description of acute high-grade rheumatic fever similar to that of Sydenham's of the late 1600's. Further, "Many of the tendons of the superficial muscles of this patient were studded with numerous small hard tumors, an appearance I have observed only in one other person...who also labored under rheumatism." Baillou recognized certain systemic features of rheumatic fever: "The whole body becomes painful, the face in some becomes red, the pain rages especially about the joints, so that indeed neither the foot nor the hand, nor the finger can be moved in the least without pain & outcry..." Later, in 1715, Raymond de Vieussens described a patient with acute rheumatic fever, since he was determined during autopsy to have a severely dilated left ventricle, the walls of the aorta were..."thick, very hard, like cartilage; the semilunar valves are markedly stretched & cut off at their tips: all these cuts which bore some resemblance to the teeth of a saw, were in fact osseous." (rheumatic valve syndrome) Later, David Pitcairn, in England, lectured, in 1788, concerning rheumatism and its affect on the heart: "...that persons subject to rheumatism were attacked more frequently than others with symptoms of an organic disease of the heart. Subsequent experience having confirmed the truth of this observation, he concluded, that these two diseases often depend upon a common cause, and in such instances, therefore, called the latter disease rheumatism of the heart." It was not until 1931 that Alvin Coburn in the USA and Wilfred Collis in England determined that Streptococcus pyogenes caused rheumatic fever, and relying on David Pitcairn's judgement, heart disease.
The above information provides the knowledge that physicians in earlier periods, back to the 1500's, used the word rheumatism, rheumatic fever, acte rheumatism and chronic rheumatism somewhat interchangeably for they knew that acute rheumatism would lead to chronic rheumatism and they also knew that a contagion, often connected with tonsillitis, or other respiratory disease presentation, could cause it. Since high-grade, acute rheumatic fever has become so rare in modern counties most currently practicing physicians have lost the clinical knowledge about it. They, therefore, have never gained the knowledge that there are lesser levels of rheumatic fever, as defined in "Osler's Principles and Practice of Medicine", published in 1935, cited above, and therefore they have even less knowledge about subacute and less than subacute rheumatic fever, which is are, semi-chronic clinical subtypes, of rheumatic fever a systemic, autoimmune-mediated, inflammatory disease.
Between 2002 and 2005 I conducted a three-year, clinical investigation in an effort to determine the true cause of most peripheral neuropathies since so many of my patients, through the years, failed to improve after they experienced spinal surgery. I eventually determined that the venerated, herniated spinal-disc concept was flawed, and most of the surgery accomplished for them was, I learned, usually mis-applied. Most patients had suspicious arthritis of the lumbar and cervical spine that featured osteophyte development and bulging of intervertebral spinal-discs, but I learned that typical MRI films did not have the resolution to "see" spinal nerve roots in an analytical fashion. Since the bulging intervertebral spinal-discs are attention-getting on MRI images, and because they do, occasionally, cause symptomatic, spinal nerve root compression, generalizing that almost all bulging intervertebral spinal-discs cause nerve root compression was a classic "red herring". After I managed to determine the cause of the painful neuropathies, I learned that the same disease that causes the neuropathies also causes arthritis of the spine; an anatomical feature of spinal arthritis, herniated spinal-discs, did not necessarily cause the painful neuropathies. There are occassional herniated spinal-discs that cause painful spinal, nerve-root compression, but surgery for them is very common.
Eventually, after a long, investigative period, I learned the most patients' neuroloical pain was caused by rheumatic, autoimmune-mediated, vasculitic neuropathy of the terminal nerves of the sacral plexus located within the piriformis canal, which is located deep in the buttock. Patients who experienced neurological shoulder/cervical pain and who experienced dysesthesias to the appropriate upper extremity, were experiencing rheumatic brachial plexitis. The brachial plexus is located within the axillary canal located deep within the shoulder. I learned that motion of the arm at the shoulder, and of the thigh at the hip, or an accident wherein either of the structures were stressed, would often cause, or exacerbate, patients' neurological symptoms and signs. Patients sensed pain in the lumbosacral region, because of centripetal referred pain from the distal sacral plexus located deep in the buttock. Similarly, they sensed pain in the cervical/shoulder region, because of centripetal referred pain from the brachial plexus located deep within the shoulder.
During the above investigation I attracted 700 miserable, painful patients who had chronic neurological pain. Eventually, I learned that they all had had meaningful, repeated Streptococcus pyogenes infections (tonsillitis, sinusitis, bronchitis, pharyngitis, otitis media, impetigo, and vaginitis) during their lifetimes and often they had experienced chronic tonsillitis. In addition, many of them, who had been born before 1970, had had, when they were younger, rheumatic fever or scarlet fever. Younger patients, born after 1970 had "flu-like" diseases with more mild symptoms and signs than accepted "Jones Criteria" standards for diagnosing rheumatic fever. I learned from information in Sir William Osler's text, Osler's Principles and Practice of Medicine, Twelfth Edition, cited above, that there are subacute and less than subacute states of rheumatic fever with more subtle systemic symptoms and signs than "classic" high-grade rheumatic fever. Such a disease has the same symptoms and signs that are thought to be those of influenza, or "the flu": a respiratory disease, often at least, lethargy, tiredness, at times stupor, body pain, back pain, photophobia, at times, headache, at times, gastrointestinal symptoms and signs, at times, and often a fairly rapid recovery. Often patients who had rheumatic fever had been diagnosed by a physician or by parents to have chicken pox, measles, the flu, mononucleosis and viral meningitis. Often the patients had been very ill, but recovered with care at home.
I conducted serology tests (ASO and Anti-DNase B titers) on over 100 patients and 70 were positive with elevated Streptococcus antibodies on one or more tests. Between the positive medical histories, the elevated serology tests, and those who had medical histories of "flu-like" diseases, chicken pox, measles, mononucleosis, and viral meningitis wherein the symptoms and signs were those of rheumatic fever, the great majority of the 700 patients, mentioned above, who had chronic neurological and arthritic pain, and other similar diseases, were qualified to have had rheumatic fever.
The great minority of cases of rheumatic fever are high-grade and qualify by the Jones Criteria to be that disease. Most cases are much more low-grade and semi-chronic in nature and such individuals develop increased, rheumatic, autoimmunological sensitivity and memory so that they are candidates, in the future, to be at risk for developing acute rheumatic fever. Current medical knowledge (Carapetis, JR.,et al., Lancet Jul 9-15; 366(9480): 155-68) indicates that an infection by a virulent strain of Streptococcus pyogenes, in a well rheumatically sensitized individual, can cause the development of acute rheumatic fever, which is known to be an inflammatory, autoimmune disease process.
The septic responses patients experienced, which frequently took place one to four weeks after an episode of respiratory disease (bronchitis, sinusitis, pharyngitis or tonsillitis) were caused by the rheumatic, systemic, autoimmune response to the autoantigens displayed by Streptococcus pyogenes. As the elevated levels of autoantibodies, and other toxic products, decreases after the peak of rheumatic fever, I hypothesize that patients maintain a low-level of rheumatic autoantibodies within themselves and it causes, over time, the signs and symptoms of chronic rheumatism. Since immunological and autoimmunological proteins circulate through the body via the elements of the circulatory system, rheumatism causes a usually subtle vasculitis, that is, arteritis, phlebitis, and lynphangitis. The much more common low-grade infections by Streptococcus pyogenes, and even the carrier state, cause an exacerbation in rheumatic stimulation, which establishes a chronic, waxing and waning autoimmune disease process within hosts, thus the chronic, autoimmune disease of rheumatism develops and is maintained.
Since Streptococcus pyogenes is endemic in human society, and a Russian Encyclopedia article (V. Nasonova & E. Talahaev) indicates that Streptococcus pyogenes is endemic in domestic vertebratres, and I hypothesize it also exists in wild vertebrates, it seems that Streptococcus pyogenes causes a universal, autoimmunological zooinosis among vertebrates including humans.
As a reminder, the terms acute rheumatism, acute articular rheumatism, inflammatory rheumatism, and rheumatic fever, all describe the same acute, high-grade autoimmunological disease caused, usually in a delayed fashion, from infections by Streptococcus pyogenes. The terms rheumatism and chronic rheumatism refers to tissue damage that usually appears minor for which signs and symptoms are often subtle, are slow evolving, and usually cause little or no dysfunction. Over time, however, they can become highly meaningful and conditions such as hip and knee arthritis, coronary artery disease, peripheral vascular disease, rheumatoid (rheumatic) arthritis, lupus erythematosis, for instance, are an indication of its severity.
The pathological anatomy of chronic rheumatism is often relatively easy to observe since, certain superficial signs of disease, for instance the articular signs of rheumatoid arthritis, dermatological features of lupus erythematosis, dermatological features of progressive systemic sclerosis, rosacea, varicosities of veins, seborrheic keratosis, various types of nevi, Raynaud's phenomenon, palmar and plantar erythema, and livedo reticularis are all manifestations of the systemic disease of rheumatism. Rheumatoid arthritis, historically, was thought to be caused by rheumatic fever. At times it has been termed, arthritis deformans. There have been other more antiquated terms for high-grade rheumatic fever and I hypothesize that two of them are sweating sickness and miliary fever.
It has not been clinically recognized, however, that all infections by Streptococcus pyogenes cause an inflammatory autoimmune response. I hypotheize that Streptococcus pyogenes infections with a high virulence is most meaningful and more frequently cause exacerbations in the rheumatic autoimmune response. In addition, the patients level of rheumatic immunological sensitivity, caused by prior infections, also contributes to the development of an energetic autoimmune response.
After various acute disease episodes, throughout life, and after numerous episode of subacute or less than subacute rheumatic fever ensues during a person's lifetime, rheumatic tissue damage slowly occurs and it eventually rheumatism manifests itself with obvious signs and symptoms of pathological damage to the body's tissues, and therefore organs, in a somewhat subtle, varying, but progressive fashion. Its manifestations are often noted as changes to the skin, tendons, ligaments, nerves and joints so clinical syndromes such as sciatica, brachial plexitis, femoral neuropathy, meralgia paresthetica, carpal tunnel syndrome, ulnar neuropathy, cardiac arrhythmias, headaches, De Quervain's tendonitis, Achilles tendonitis, olecrannon bursitis, rotator cuff abrasions and tears, and Dupuytren's contracture appear. One must remember, however, that rheumatism is a systemic disease process so that all tissues, and therefore organs, are pathologically affected. Therefore, arteriosclerosis, endocrinopathies, renal failure, asthma, allergies, inflammatory bowel syndome, primary sclerosing cholangitis, pancreatitis, osteoporosis, spastic bladder, schizophrenia, obsessive-compulsive behavior, depression, and many, many other pathological conditions are caused by rheumatism. "One must think: each tissue, and therefore each organ, will clinically express the adverse effects of the systemic disease of rheumatism in its own way, thus, many apparent separate diseases develop, over time, in a somewhat random, but often connected, fashion."
High-grade rheumatic fever decreased in incidence starting in the early 1900's within modern, industrialized societies, secondary to the improvements in living conditions which were brought on by advances of basic science that begot the industrial revolution. Advances included larger homes and smaller family size, both of which caused decreased crowding within dwellings, which decreased the spread of Streptococcus pyogenes within families. In addition, more hygienic living habits, the common use of soap, improvements in home bathing facilities, the use of clothes washers, dish washers, and the pasturization of milk all contributed to a decreased spread of Streptococcus pyogenes within society. Later, in the 1930's, the use of broad spectrum antibiotics for respiratory infections was initiated. The environmental changes, and the common use of antibiotics, resulted in fewer and fewer Streptococcus pyogenes infections, but more importantly, perhaps, infections with less virulence, so by 1970 high-grade rheumatic fever was a relatively rare disease in modern, developed countries. Chronic rheumatism also decreased in severity in especially in younger populations, but it still appeared, as a pathological entity, in older people as they lived through the years.
Unfortunately, in 1987 rheumatic fever experienced a resurgence with the first reports appearing in The New England Journal of Medicine with the author, L. George Veasy, MD wrote about a mini-epidemic from the area around Salt Lake City, Utah. Thereafter, numerous mini-epidemics have been reported from many areas in the USA. A mini-epidemic of acute rheumatic fever took place in Lewis and Cowlitz Counties of Washington State during the winter and spring of 2004 and 2005. A few people patients died before that period from rheumatic fever, but I didn't recognize it, but about ten people died out of my patient population of about 7000 during the aforementioned period. A number of patients have died thereafter who lived in the same geographic area. The individuals who died were fairly young, in their thirties to their sixties, they all experienced chronic neurological pain and arthritic symptoms, three of them had had a history of previous rheumatic fever or scarlet fever (Scarlet fever is the same disease as rheumatic fever, except it is caused by a separate sub-species of Streptococcus pyogenes, which develops a somewhat specific rash.) , a number of them had experienced spinal surgery with no improvement in symptoms or signs, and they were taking opiates for their severe, chronic, neurological pain when they died. Unfortunately, the local coroners, neither of whom had much medical knowledge or wisdom, made a determination that some of the patients died from the affects of opiates that they were taking for their chronic rheumatic pain. Some of the patients, on whom I had accurate information, had classic signs and symptoms of acute rheumatic fever so they qualified, by the Jones Criteria, to have had severe, acute, rheumatic fever. They had enlarged hearts and pulmonary edema on autopsy as an indication that they had had acute rheumatic carditis (myocarditis and endocarditis).
One of the painful, clinical, rheumatic conditions, which many children commonly experienced in somewhat earlier times, such as before the 1970's, was growing pains. Growing pains manifest themselves as a painful sensation in the legs, commonly the thighs and knees, and it develops, often, shortly after going to sleep, or lying down, and wakes the young patient who often complains, and even cries, due to the severity of pain. Other clinical manifestations of rheumatism, which children experience, are torticollis (wry neck) and dorsodynia, which is an older term for upper back pain that is usually felt in the scapular region, which, I determined, is frequently a referred pain pattern caused by rheumatic brachial plexitis. Another syndrome children experience, occasionally, is Kawasaki disease. I surely think that Kawasaki disease is a syndrome that is a presentation of rheumatic fever in a child who is "well conditioned" to have a severe rheumatic vasculitic response by having experienced a number of Streptococcus pyogenes infections earlier in life. They could have experienced a chronic infection, which caused an elevated sensitivity to the autoantigens of a virulent subtype of Streptococcus pyogenes. Another syndrome that adults contract is Guillain-Barre' Syndrome. It is a presentation of rheumatic fever wherein the individual experiences an acute, systemic neuropathy and paralysis at some level. Usually they experience a respiratory infection somewhat before their attack and such a pattern of delayed autoimmune disease is classic for Streptococcus pyogenes infections and their delayed rheumatic response.
Simultaneously with the above changes in the frequency of high-grade rheumatic fever, the citizens of modernized countries experienced a steadily advancing life-expectancy; in the USA life expectancy increased from forty-seven in 1900 to about seventy-seven in 2000: an increase of about thirty years, which equates to an increase of 64% over a 100 year period. There has to be a logical reason for the increased longivity. The reason, mainly, I hypothesize, has been a decrease incidence, and severity, in general, of Streptococcus pyogenes infections; a generally decreased level of virulence of Streptococcus pyogenes itself, which resulted in a great decrease in the incidence of acutge rheumatic fever and, therefore, chronic rheumatism decreased in severity in the populations of economically advanced countries. The decrease in the incidence of acute rheumatic fever, a disease that often caused the death of children and younger people, greatly contributed to the increase in human life-expectancy. There were other positive factors also, for instance, a better food supply, vaccines for other diseases, and improved medical care, especially supportive care and disease altering surgical procedures.
Rheumatic autoimmunity causes, initially and continually, an inflammatory vascular condition, which is its main pathological mechanism, that results in inappropirate intra-arterial thrombosis especially at arterial bifurcations. The immune system reacts to localized intra-arterial thrombosis with an enhanced, localized inflammatory response so that inflammatory, intra-arterial, arteriosclerosis lesions develop. As Streptococcus pyogenes infections decreased, as mentioned above, fewer myocardial infarctions developed early in life and coronary artery disease became, to a great degree, a disease of older people, in modernized portions of the world, since it is caused by more subtle, chronic rheumatic autoimmune condition: chronic rheumatism.
In 1931 Coburn in the USA and Collis in England determined, somewhat simultaneously, that Streptococcus pyogenes caused rheumatic fever, but professional inertia being what it is, many physicians did not completely accept their theory until the late 1940's and the early 1950's when rheumatic fever, as a high-grade disease, was becoming less and less common, primarily, because of the above-mentioned improved living conditions and use of antibiotics mentioned above.
Starting in the 1920's, slowly, but then accelerating, especially in the 1950's, medical practice and education became conceptually segregated by means of specialty-organized, procedure-dominated concepts and by the 1960's most physicians were specialists and specialty practice settings and knowledge-states were not conducive to an understanding of systemic diseases. Since acute rheumatic fever, and moreso, chronic rheumatism are basically the same disease, with the former being an acute exacerbation of the latter, the latter, chronic rheumatism, which has a multitude of target-organ manifestations, simply was not recognized, or ceased to be recognized, by the members of the specialty-oriented medical community.
Individuals in the various surgical specialties concentrated on various target-organ manifestations of rheumatism and developed disease-altering cardiac, surgical procedures such as CABG surgery, angioplasty/stent procedures, cardiac valve modification and replacement procedures, and cardiac arrhythmia altering surgery, etc. Surgical procedures to alter, usually for the better, rheumatic pathology to gastrointestinal organs consist of, in part, surgical procedures such as cholecystectomy for cholecystitis, various surgical procedures for ulcerative colitis, redundant colon, Crohn's disease, esophageal strictures, primary sclerosing cholangitis, and gastric and peptic ulcers. The latter two, gastric and peptic ulcers are primarily caused by rheumatic vasculitis, but that condition is exacerbated locally by Helicobacter pylori infection. In general, infections cause a localized exacerbation of rheumatic vasculitis. In addition, organs that function peristaltically, as do most of the gastrointestinal organs, feature compression and abrasion of tissues, which also causes an exacerbation of rheumatic vasculitis, in a semi-localized fashion, within them. Pyrosis, or heart burn, is another clinical entity caused by rheumatic vasculitis. The peristaltic compression causes enhanced rheumatic vasculitis, which is further exacerbated, usually in the distal esophagus, by the effect of hydrochloric acid and digestive enzymes from the stomach on the esophageal endothelium.
In addition, many chemotherapeutic medications were developed so the use of NSAIDS, steroid anti-inflammatory medications, artery dilators, cancer chemotherapy drugs and countless other chemotherapeutic drugs became commonly used to alter the affects of chronic rheumatism on various organs. Both NSAIDS and steroid anti-inflammatory medications are used for acute, rheumatic fever, in addition.
During the development of "specialty medicine", it seems that rheumatology, one of the last specialty groups organized, was "elbowed" into dealing with only connective tissue, perhaps since other groups of physicians had claimed authority of the other organ systems, although most rheumatic syndromes such as rheumatoid arthritis, lupus erythematosis and psoriasis, for instance, are known to be systemic disease processes. The specialty-medicine paradigm that developed, since the 1920's, simply never provided a systemic disease concrept-base so chronic rheumatism has never been understood in a modern, etiological fashion even though all the clinical elements of its understanding had been provided by investigators in prior eras, by the microbiological breakthroughs of the late 1800's through the early 1900's, and by the insights made concerning autoimmune disease concepts. A valuable text that provides a current understanding about the current state of knowledge about autoimmunity is, "The Autoimmune Diseases" Fourth Edition (Rose, N., Mackay, I., Academic Press, 2006).
Even though high-grade rheumatic fever greatly decreased in incidence after1900 lesser levels of rheumatic autoimmunity have still been propagated throughout human society, including modern developed countries, since Streptococcus pyogenes infections still exist endemically, but usually with less virulence, within the populations of all countries. Therefore, since Streptococcus pyogenes infections are endemic at any one time, at some level, in all communities in the world, at some level. For instance, the non-symptomatic carrier state of Streptococcus pyogenes is between 5%-15% of grade school children as per information in the text, "Rheumatic Fever and Streptococcal Infection", cited above. Hypothetically, low grade infections will cause low-grade autoimmunological stimulation within those very mildly sick individuals and they can pass infections on to those around them.
The clinical understanding of high-grade rheuamtic fever (acute rheumatism) decreased in modern countries so that, nowadays, in the USA, the average physician has virtually no, or little, knowledge of acute rheumatic fever at this time. Knowledge, therefore, of the much lower-grade, chronic, rheumatic autoimmunity and its more subtle, slowly-developing, target-organ manifestations has never been developed in modern medical science and along the way, rheumatism as a chronic disease concept, was dismissed as a serious medical subject, even though, as early 200 AD, certain knowledge concerning rheumatism was known, and in the late 1700's the "clinical features" of acute and chronic rheumatism was reasonably well known.
For instance, Galen, the famous Greek physician in the Roman period, who published over 66,000 pages of medical, philosophical, and scientific information, half of which has managed to survive since 200 AD, coined the word rheumatismos. Rheum, in Greek, means to flow, or phlegm. The phrase "a defluxion of rheum" could be used. It was later connected with catarrh, influenza, or the grippe, terms that describe a respiratory disease. Galen knew, I hypothesize, that when people developed contagions that caused the development of phlegm, and, perhaps, chronic phlegm development, they would also, eventually, develop chronic, painful problems that were part of the chronic disease of rheumatism. Arthritis, neuropathy (such as sciatica, carpal tunnel syndrome, ulnar neuropathy, brachial plexitis, for instance), angina, pericarditis, pleurisy, tendonitis, ligamentitis (for instance plantar fasciitis) are examples of modern names for target-organ manifestations of rheumatism.
As mentioned above, within the first edition of the Encyclopedia Britannica, cited above, on page 124, under the chapter on "Medicine", under the paragraph, "Of the Rheumatism", a description of acute rheumatic fever similar to that written by Thomas Syndenham, during the 1600's, is provided. It mentions fever, chills, rapid heart rate, fatigue, lassitude, gastrointestinal problems, sciatic pain (lumbago), and migratory arthritis. It saliently mentions, "The proximate cause is the inflammation of the lymphatic arteries." Further, it mentions, "The chronic rheumatism is either the remains of a rheumatic fever, or a continuation of pains that proceeded at first from lesser but neglected colds."
It appears, clearly, that physicians in the mid-1700's knew that the "Proximate cause (or pathological finding) was inflammation of the lymphatic arteries (arteries) a condition now known as vasculitis, phlebitis, and lymphangiitis. Of course the rheumatic vasculitis that exists in those with chronic rheumatism is somewhat low-grade. They also knew that repeated "...lesser but neglected colds." could cause the systemic disease of rheumatism, but in the modern day, pundits of evidence-based medicine (whose evidence, how was it gathered, who interpreted it?) pontificate to student-physicians that, all "colds" are caused by viruses so upper respiratory diseases, even sore throats and tonsilitis, are not to be treated with antibiotics unless a positive quick strep test or culture is positive. Unfortunately, such tests are often inadequate or inconclusive and since Streptococcus pyogenes can exist intracellularly within the epithelial cells of the pharynx, and even "within" the tonsils, in which case quick Strep tests and cultures will usually, or often, be negative. (Rheumatic Fever and Streptococcal Infection, cited above) One must remember that when a physician is dealing with Streptococcus pyogenes infections one is dealing with a very important aspect of a patient's health.
The term "rheumatism" is still used in colloquial speech and in historical contexts, but it is no longer frequently used in medical or technical literature; it would be fair to say that there is no longer any recognized disorder simply called "rheumatism". The traditional term covers such a range of different problems that to ascribe symptoms and signs to rheumatism, would violate, more than trivially, the artificially developed specialty structure that has developed in modern, western medicine since the 1920's.
One of the first organizations that dealt with rheumatism, in the modern day, was the European League Against Rheumatism. Unfortunately, rheumatologists, to maintain their specialty-mandated specialty status as experts at connective tissue diseases, do not generally deal with infectious diseases or problems of the body's organs even though they also, historically, have dealt with rheumatic fever, which is a high-grade, inflammatory, autoimmune-mediated, systemic disease process stimulated by Streptococcus pyogenes infections and that most "rheumatic diseases" such as rheumatoid arthritis and lupus erythematosis are systemic diseases, per se.
As a vestige of past wisdom, many individuals knew that arthritis, neuropathy, tendonitis, dermatological problems, and many other adverse health conditions had something to do with rheumatism. For instance, during the early 1900's, in America, sciatica was termed sciatic rheumatism or hip gout, eczema of the hands was termed, salt rheum, and gout was termed, gouty rheumatism. Those who understood the collective wisdom of the time knew that the maladies described were part of the rheumatism complex. Old farmers, walking bent over with a cane often have said, "Oh, my rheumatism". Non-articular rheumatism, also known as soft tissue rheumatism, and which is now known as "fibromyalgia", was in prior eras known as "muscular rheumatism". Somewhat surprisingly, that variously described condition is a dispersed rheumatic, sensory neuropathy: bilateral brachial plexitis, sacral plexitis and at times femoral neuropathy that is made more symptomatic by use of the arms and legs. To understand the above pathophysiology an examiner must do an analytic, neurological examination of the brachial plexus, the terminal nerves of the sacral plexus, and the femoral nerve; they must "know" the location of the dermatomes of the body: in SPADES.
Within the chapter on rheumatoid arthritis in Harrison's Principles of Internal Medicine, 16th Edition, cited above, the "NUT" of rheumatism is presented. The author's provides an interesting description: "Rheumatoid arthritis is a chronic multisystem disease of unknown cause." Further, the following is mentioned: "In approximately 10% of individuals the onset is more acute, with a rapid development of polyarthritis, accompanied by constitutional symptoms, including fever, lymphadenopathy, and splenomegally." It describes that rheumatoid arthritis features arthritic aspects, rheumatoid nodules, vasculitis, neuropathy and organ infarction, even myocardial infarction. At times, the text indicates, "Neurovascular disease presenting either as a mild distal sensory neuropathy or as mononeuritis multiplex may be the only sign of vasculitis." Anemia, subcutaneous nodules, and osteoporosis are concomitant features of rheumatoid arthritis. It mentions that pericarditis is found in 50% of individuals with rheumatoid arthritis at autopsy.
Referring to the above description of the "...chronic multisystemic disease..." of rheumatoid arthritis, many signs and symptoms are identical to those found in rheumatic fever: subcutaneous nodules, a feverish disease that exists somewhat before arthritis develops, lymphanenopthy, polyarthritis, splenomegally, vasculitis, neuropathy and organ infarction are all found in acute rheumatic fever patients and some sequelae are found in those with chronic rheumatism.
The connections, mentioned above, of a mild, acute disease triggering vasculitis, arthritis, neuropathy, myocardial infarction, anemia, pericarditis, and osteoporosis describes many of the same pathological features that are historically attributed to rheumatism. The acute disease process mentioned, is, I surely think, a subacute case of rheumatic fever (the type Sir William Osler described in his famous text of 1935), the pathological, systemic, inflammatory, autoimmune disease that post-dates, from a week to five weeks, the Streptococcus pyogenes infection that cased it.
Within the text, Rheumatic Fever and Streptococcus Infection, cited above, the author indicates that fifty percent of Streptococcus pyogenes infections that trigger rheumatic fever have such mild symptoms and signs that patients do not remember them when queried, therefore, it would not be surprising that low-grade respiratory infections and even the somewhat higher grade infections would be missed, forgotten, or just thought to be important.
Individuals who develop high-grade rheumatic fever are often thought to have developed a different, and separate, idiopathic (meaning the cause is not known), acute disease process, but it also has symptoms and signs of vasculitis, arthritis, pericarditis, subcutaneous nodules (which develop due to chronic rheumatism), fever, splenomegally, lynphadenopathy, at times enlargement of the cervical lymph nodes, renal abnormalities, hepatitis, delirium, neuropathy, epistaxis, urticaria (hives) or other rash, and other systemic symptoms and signs, which vary significantly, depending on the severity of the individual disease episode.
Individuals who experience severe cases experience severe pain. Sir William Osler has written the following concerning the pain experienced by patients who have high-grade rheumatic fever: "Perhaps no disease is more painful; the inability to change posture without agonizing pain, the drenching sweats, the prostration and helplessness, combine to make it a most distressing affection ("Osler's Principles and Practice of Medicine, Twelfth Edition, cited above). I learned from experience that when individuals experience severe rheumatic fever, with its severe pain, they will take any thing in an effort to decrease it: opiates, aspirin, ibuprofen, alcohol, cold remedies, etc. Since they become delirious they may behave unwisely and/or behave nastily to those around them. Many patients who die from rheumatic fever, in the past, have been experiencing chronic rheumatism with one of its symptoms being chronic neuropathic pain. Not unusually, they have been prescribed chronic opiates so when they become sick with recurrent rheumatic fever and die, usually at home, their deaths are "blamed" on the opiates they took. A tell-tale sign on examination is, often, however, pulmonary edema and an enlarged heart about 20% above normal. In addition, they often will have a history of a respiratory disease, or a "flu-like" disease, concomitantly or a few weeks before. Possibly, celebrities such as Brittany Murphy (who had the autoimmune target-organ disease of diabetes, her husband (rheumatic fever tends to be a family disease, because Streptococcus pyogenes is very contagious among close-living individuals), Cory Haim, Heath Ledger, Michael Jackson (who had the autoimmune syndrome of vitilago and, perhaps, his quick, stuttering dance steps were, in part enabled by
"Rheumatic fever has various serious manifestations, for instance, carditis, endocarditis (heart valve malfunction), pericarditis, clinical heart failure heart failure, pulmonary edema, rheumatic pneumonitis and cardiac arrhythmias. In addition, it features lassitude, stupor, coma, chorea, and, at times, seizures caused by rheumatic encephalitis. Further, patients experience abnormal kidney function leading to kidney failure, at times; chronic rheumatism is a cause for chronic renal failure. Since rheumatic carditis is a life-threatening target-organ manifestation, and since acute rheumatic myocarditis, endocarditis, pericarditis, and cardiac arrhythmias are aspects of its spectrum, most medical attention in acute rheumatic fever cases is, logically, given to the heart, but in truth, it is a systemic disease process.
For a long period, most medical attention connected with acute rheumatic fever is focused on chronic cardiac valve disease. It is known that individual patients who have had rheumatic fever in the past may have chronically developed cardiac valve abnormalities, with the mitral valve the most commonly abnormal. Most cardiologists, in the modern day, specialize in disease altering procedures to alter the disease of the heart; and they rarely think about, or clinically deal with, acute, systemic, rheumatic fever. The rest of the target-organ manifestations of rheumatic fever have been, more or less, inappropriately disconnected from the acute, disease process and the disease diagnosis that is provided depends on what type specialist attends the patient. If they have meaningful hepatic problems, they may be deemed to have a type of hepatitis. If they have renal failure as a major problem, they may be diagnosed to have acute renal failure. If they have pulmonary failure they may be diagnosed to have interstitial pulmonary disease or, simply, pulmonary failure. Even if they have highly meaningful cardiac problems cardiologists often make the diagnosis of acute heart failure and pulmonary edema, but do not deal with the condition with an etiological approach. The physician, in the modern day, it seems, has the job of providing a "diagnostic code" approved by insurance companies; that is all that is really needed....to get paid.
Like most diseases, rheumatic fever (acute rheumatism) exists as a lower-grade, subtle disease phenomenon most of the time, and relatively rarely, except in certain, favorable epidemiological situations, does rheumatic fever exists in the high-grade state that has the symptoms and signs popularized by the Jones Criteria. Surprisingly, T.Ducket Jones, MD, who invented the Jones Criteria, did not think that Streptococcus pyogenes was the cause of rheumatic fever even in the early 1950's, although, as mentioned above, Alvin Coburn published a monologue that provided proof that it did, in 1931. To keep using the Jones Criteria, nowadays, is improper, I surely think. To think that rheumatic fever is mainly a cardiac disease is also a gross error: it is a systemic, autoimmune disease process, which in high-grade cases has serious, acute, somewhat focused, cardiac, autoimmunological target-organ manifestations.
The rheumatic diseases, which are caused by the autoimmunological response to infections by Streptococcus pyogenes (and perhaps other Streptococcus species) include rheumatoid (rheumatic) arthritis, psoriasis and its arthritis, lupus erythematosis, Sjogren's syndrome, scleraderma, ankylosing spondylitis, dermatomyositis, myositis, Wegener's granulomatosis, and osteoarthritis. They are caused by the autoimmune response to Streptococcus pyogenese infections during the patients' lifetimes. Osteoarthritis is simply rheumatic arthritis that appears in certain joints such as the spine, knees, hips, and hands due to a localized, exacerbation of rheumatic vasculitis that is caused by the mechanical factors of compression and abrasion. For instance, the first three locations feature exacerbated arthritis somewhat commonly due to the compression and abrasion experienced by the joint structures during weight bearing and active use. Individuals' hands, especially womens' hands, often feature arthritis, commonly termed osteoarthritis and rheumatoid arthritis, which are really the same disease state, due to the individual's frequent use, which involves compression and abrasion of the joints, tendons, ligaments and soft tissues of the hands. Also, heat and cold, in general, also cause an exacerbation of rheumatic inflammation in a local fashion. Women are thought to have rheumatoid (rheumatic) arthritis more often then men. Perhaps women use their hands in a more intense and common fashion than most men in the modern day as they do housework and yard work.
Peripheral neuropathies such as lumbosacral/buttock pain with sciatic pain referred down the leg; it is caused by rheumatic inflammation to the terminal nerves of the sacral plexus the sciatic, posterior femoral cutaneous, pudendal nerves. Femoral neuroapthy, carpal tunnel syndrome (median neuropathy), cubital tunnel syndrome (ulnar neuropathy), peroneal neuropathy (lateral lower leg and foot), meralgia paresthetica (neuropathy of the lateral femoral cutaneous nerve), and tarsal tunnel syndrome are all aspects of rheumatism. Fibromyalgia is a dispersed neuropathy of the bilateral brachial plexus, the terminal nerves of the sacral plexus and femoral nerve, and other nerves). Femoral neuropathy can present in a clinically isolated fashion. Various cranial neuropathies such as trigeminal neuropathy can appear as facial pain or the many branches to the meninges can be primarily affected, which, hypothetically, can cause migraine headaches and other clinical types of headaches. Bell's palsy (rheumatism of the facial nerve), hearing deficits, vertigo, Menier's disease, and abnormalities of the motor nerves of the eye are all caused by rheumatic autoimmunity. When neuropathies present more severely they are more systemic in nature so they manifest as the syndromes of multiple sclerosis, Guillain-Barre' syndrome, and, hypothetically, amyotrophic lateral sclerosis.
Rheumatic endocrine abnormalities are common, for instance, diabetes, Addison's disease, Cushing's syndrome, hypothetically, polycystic ovary disease, testicular failure, hypothyroidism, Hashimoto's thyroiditis, hypoparathyroidism, and pituitary abnormalities of various types are usually, more likely, caused by rheumatic autoimmune attack. Hypothetically, children with diabetes probably experienced acute rheumatic fever and the, more or less, acute development of diabetes is one of its sequelae. The others, mentioned above, are due, usually, to chronic rheumatic attack that is caused by rheumatic fever as well as by, or inaddition to, lower grade Streptococcus pyogenes infections during their lifetimes.
Benign Tumors and cancer of various types are rheumatic in nature. Nevi (moles) of various types, freckles, seborrheic keratosis, and many more lesions, usually thought to be benign, are secondary to pathological rheumatic stimulation. Cancer of all tissue types are target-organ manifestations of the systemic autoimmune disease of rheumatism. The rheumatic neuropathies (written about two paragraphs, above) often appear before, or concomitantly, with cancer and they are termed, in that case, paraneoplastic neuropathy. Often the neuropathy is sciatica or the individual has a history of sciatica. Ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, gastritis and esophagitis are also autoimmunological manifestations of rheumatism and like many "systemic rheumatic conditions" such as dermatomyositis and lupus erythematosis, they are also paraneoplastic conditions. I estimate that most individuals who develop cancer have, at least, rheumatoid (rheumatic) arthritis at some level of severity so it, hypothetically, can be thought to be a paraneoplastic, rheumatic disease presentation, also.
Since rheumatism is, first of all, a vascular disease peripheral artery disease of the extremities, carotid stenosis, aneurysm development, CVA's, and kidney vascular abnormalities are all, usually, caused by rheumatic vascultis, the primary lesion of rheumatism. Phlebitis, usually in the lower extremities, is also a manifestation of rheumatic autoimmunity. Lymphedema is probably a condition caused by rheumatic autoimmunity.
Rheumatic central neuropathic conditions are highly variable due to the complexity of the spinal cord and the brain. In recent years there have been breakthroughs that show the "tip of the iceberg, so to speak, in that PANDAS (Pediatric Autoimmune Neurological Deficits caused by Streptococcal infection) is a concept that has wide appreciation. The clinical syndromes, autism, ADHD, Tourette's syndrome (tics, stuttering, stammering, antisocial behavior, explosive personality, coprolallia, echolallia, dysinhibition, etc.), depression, schizophrenia, manic-depressive illness, and disassociative reactions are some manifestations of "rheumatism of the brain", as it were termed in an earlier era.
Gastrointestinal system: target-organ maladies: ulcerative colitis, Crohn's disease, celiac disease, primary sclerosing cholangitis, pancreatitis, peptic ulcers, gastric ulcers (Helicobacter pylori is just an exacerbating problem with rheumatic vasculitis), esophagitis, peridontal disease.
Bursitis: olecrannon bursitis, pre-patellar bursitis, tibial tuberosity bursitis (house maids knee), and subacromial bursitis are examples.
Tendinitis: tendonitis of the long head of the biceps, DeQuervains tendonitis, Achilles tendonitis, and rotator cuff abrasions, tears, etc. Ligamentitis such as plantar fasciitis, deltoid ligamentitis of the medial foot, etc.
Cardiological rheumatic problems: rheumatic cardiac valve syndrome, coronary artery disease, acute and chronic myocarditis (LVH, global cardiac enlargement, and decompensated enlarged heart), pericarditis, and cardiac arrhythmias are all caused by rheumatism. Coronary artery disease and another cardiac problems were termed, "rheumatism of the heart" a concept that was developed by David Pitcairn in 1788 (Rheumatic Fever and Streptococcus infection, cited above).
Kidney: rheumatic vasculitis leading to chronic rhenal failure, gout, and kidney stones.
Special Senses: cataracts, retinitis, iritis, keratokornus, uveitis, subconjuctival hemorrhage, decreased hearing, tinnitis, Menier's syndrome, phorias, tropias, and hyposmia are examples.
Skin: seborrheic keratosis, dermatitis, nevi, angiomas, purpura, urticaria, telangectasias, rosacea, erythroderma, poliosis, vitilago, spider nevi, petechiae, actinic keratosis, Stevens-Johnson syndrome, hypothetically, pityriasis rosea, palmar erythema, plantar erythema, dermographism and others.
Although the above disorders usually are not thought to have much in common etiologically, they are all target-organ manifestations of one variable, inflammatory, autoimmunological disease process: rheumatism. One cannot expect the eye to respond to a systemic disease as the plantar facia responds. One cannot expect the medial meniscus to respond to a systemic, inflammatory disease as the hip joint responds. One should not expect the brain to respond to a chronic, inflammatory, autoimmunological condition as the heart responds. All rheumatic conditions are inflammatory in nature and share two characteristics: they cause chronic (though often intermittent) pain, and they are difficult to treat. They are also, collectively, very common. Aspirin, other NSAIDS, and streroid antiinflammatory medications are used, however, to treat many of them and they "work" reasonably well if taken in adequate doses for protracted periods. Even coronary artery disease, and recently cancer, at times, are prophylactically treated with aspirin.
Since acute rheumatic fever causes a dampening of the protective immune response, hypothetically the innate immune response, "other" infections often develop with acute rheumatic fever (as enumerated by Sir William Osler in his text, Osler's Principles and Practice of Medicine, Twelfth Edition, cited above. Tuberculosis, diptheria, cholera, whooping cough and other diseases are mentioned. Chronic rheumatism also causes a decreased immune response and I surely hypothetically think that tuberculosis, MRSA, Streptococcal necrotizing fasciitis, erysipelas, Lyme disease, herpex zoster, mononucleosis, AIDS, possibly Chigas disease and malaria, are all infectious disease process that take place more commonly in individuals who have high-grade rheumatic autoimmunity: rheumatism.
One can consider that rheumatic fever itself is also an acute aspect of rheumatism and its former name, acute rheumatism, more or less, defines that concept.
interested physicians should read articles and texts by Gene Stollerman, M.D. and Benedict Massel, M.D., two of the last physicians who treated many, patients who had rheumatic fever. Dr. Stollerman has written that physicians should treat patients with pharyngeal infections, after clinical inspection provides a reasonable adjudication that Streptococcus pyogenes could be the causual micorbiological agent, with penicillin. No wonder the American population is becoming populated with millions of cases of fibromyalgia (muscular rheumatism), diabetes, sciatica, autism, MS, cancer, cardiac disease, psychological diseases, and other conditions. One aspect of rheumatic encephalitis is Tourette's syndrome and one of its aspects is antisocial behavior. Our prisons are "filled" with hundreds of thousands of inmates, usually the poorer class of person, who is more likely to have experienced rheumatic fever, and many of them have organic mental problems caused by rheumatic encephalitis.
Since modern, specialty medicine "missed out" on recognizing rheumatism as an abiding, systemic, inflammatory disease that all humans develop, it evolved the concept that the target-organ manifestations of chronic rheumatism were independent idiopathic diseases. The semantic error of using the term disease, when the cause of a malady is not known, led, I surely think, to the general self-deception that physicians knew more about diseases than was true: they were dealing with syndromes, symptom and sign patterns, and not well defined diseases wherein their causes are known. Coronary artery disease is really coronary artery syndrome, for instance. Crohn's disease is really Crohn's syndrome and the list can go on and on since the great majority of the descriptions of "diseases" that fill medical texts such as Harrison's Principles of Internal Medicine, 16th Edition, cited above, are really syndromes: symptom and sign patterns that commonly appear together. Medical science, has, therefore, for the last sixty years developed a multitude of disease altering treatments for various diseases and not curative treatments since the cause of a disease must be known before definative cures can be developed. Modern clinical trials are organized efforts to find a chemical that will alter, significantly, a syndrome for the better; not to cure a disease.
To better understand "where medical science is" at this time, an individual must understand the the scientific revolution of thought started in the modern era, about 1600, and that a modern approach to medical science was not possible without the insights first developed by Antony van Leewenhoek concerning microbiology. Progress was slow, thereafter, so that in 1850, just two long life-times ago, physicians did not know the cause of one disease so all treatments were disease altering. If a patient did not have a laceration, a fracture or a sprain, conditions wherein the cause was known, no curative treatments could be managed. Then the microbiological revolution started in Germany and France with the work of Pasteur, Henle, Koch, Ehrlich, and others. Their breakthroughs stimulated American medical science to become more academic. By the late 1930's sulfonamide and penicillin had been developed and their use was a great boon to physicians and patients alike. It seemed that there was not much further worry about infectious diseases and physicians and medical researches dropped their guard, understandibly.
Autoimmune concepts had been developed early in the 1900's, but the excitement over microbiology and antibiotics and the development of specialty, procedural medicine caused interest in immunology to wane. Interest in immunology re-developed in the 1970's and great progress has been made, but there have been few physicians on the street seeing patients of both sexes, of all ages, and for all diseases, who happened to practice in an area where rheumatic fever was active, and who could put the advances in immunology together, at least in a superficial fashion, with clinical medicine. I hope I have succeeded.
Treatment
Since the etiolgy of rheumatism has not been known, individuals throughout history have used a great number of traditional and more modern treatments for the many symptoms of rheumatism. Modern medical treatment often consists of non-steroidal anti-inflammatory treatments and steroid anti-inflammatory treatments. Both are used for acute, rheumatic fever also. Treatment for the target-organ manifestations of rheumatism are as varied as cryotherapy for dermatological lesions, both cancerous and benign, surgical treatment for rheumatic arthritis as of the knees and fingers, tendonitis of the rotator cuff, and spinal surgery for heriated spinal-discs, which is usually inappropriate. Aaron Filler, M.D. (backpain-guide.com) accomplishes piriformis canal enlargement procedures to decrease the pressure on the terminal nerves of the sacral plexus and often has good results from his procedures when individuals experience recalcitrant sciatica.
Somewhat commonly, initial therapy for mildly painful symptoms of rheumatism is to use non-opiate analgesics such as acetaminophen. Since rheumatism is an inflammatory disease process, of an autoimmunological nature, non-steroidal anti-inflammatory/analgesic medications (NSAIDs) are used, some members of which are aspirin, ibuprofen, naproxen sodium, indomethocin, and diclofenac. Many others exist. Often, more efficacious analgesics are required and if individuals have meaningful pain, opiate analgesics have been safely used for hundreds of years.
Most patients will experience a relief of thier severe neurological pain if they are provided a Steroid injection such as triamcinolone 80 mg. intramuscularly via the upper outer quadrant of the buttock. They should experience reasonable relief in three to four days. They should take aspirin, 325 mg, coated, three times a day and indomethacin 25 mg. three times a day, together, also, and also take ranitadine, 150 mg a day to decrease stomach acid production.
The current practice of providing steroid injections into the spinal space is not needed, because even when it is injected in that area (by an expensive procedure), it will be absorbed by the arterial and venous circulation and spread around the body: it does not matter where it is given and so an intramuscular injection is adequate as long as the dose is high enough. I surely think, for a short period, like three months, a triamcinolone injection can be given every three weeks, or so.
At times a family member, or the patient, can be a Streptococcus pyogenes carrier so I used to see all immediated family members living in the same house and treat them all for a short time with an adequate dose of penicillin.
If individuals know they have had rheumatic fever, or if they have positive or high normal serology tests for Streptococcus pyogenes, ASO, Anti-DNase B, Anti-hyaluronidase, Anti-Streptokinase, for instance, prophylactic use of penicillin VK, G, or amoxicillin can be used to decrease the frequency of high-grade rheumatic fever, by decreasing meaningful Streptococcus pyogenes infections. Keflex or Erythromycin can be used if a person is allergic to penicillin. Certain organizations are working on the development of a vaccine for Streptococcus pyogenes.
"Rheumatism" and weather
For a long period, it has been suspected that there is a link between "rheumatic" pain and the weather. There appears to be no firm evidence in favour or against that idea, but a 1995 questionnaire given to 557 people by R. Jamison, and others, at the Brigham and Women's Hospital's Pain Management Center concludes that "changes in barometric pressure are the main link between weather and pain. Low pressure is generally associated with cold, wet weather and an increase in pain. Clear, dry conditions signal high pressure and a decrease in pain"[2].
Within the first edition of the Encyclopedica Britannica, the following quote is provided: "The rheumatism chiefly attacks persons in the flower of their age, after violent exercise, or a great heat of the body from any other cause an, and then being too sudenly cooled."
Within the text, Rheumatic Fever and Streptococcal Infection, cited above, the following is written: "Haygarth in 1805 was one of the earliest physicians to relate rheumatic fever to the throat when he noted that "persons who have been previously affected with the acute or chronical Rheumatism, the Gout, or sore throat, especially the first, are most liable to suffer attacks of this disease; and ought therefore to be particularly careful to avoid exposure to cold and moisture." In a study of 175 patients with acute rheumatism he observed that sixty-five of them ascribe their disease to "having caught a cold" and he expressed the opinion that the exciting cause was "exposure to cold and moisture.""
Within Sir William Osler's text, published in 1912, cited above, within the section of chorea the following is mentioned, "The cases are most numerous when the mean relative humidity is excessive and the barometric pressure is low (Lewis). Concerning rheumatic fever in the same text, "It prevails in temperate and humid climates...The disease prevails in the more northern latitudes...The general impression is that the disease prevails more in the British Isles than anywhere else...In Norway, where cases of rheumatic fever are notified, there were, for the four years 1888-'92, 13,654 cases, with 250 deaths.,,CHILL--Exposure to cold, a wetting, or a sudden change in temperature are among the factors in determining the onset of an attack, but they were present in only 12 per cent. of our cases.
It is well known by mothers and physicians that respiratory diseases, colds, are more common in the autumn, winter and spring and those are the seasons when rheumatic fever is most common. In the above mentioned text, Rheumatic Fever and Streptococcal Infection, cited above, Bernard Schlesinger indicated, " It is no exaggeration to say that acute nasopharyngeal infection is the most serious menace to the rheumatic child with heart disease."
I do not think barometric pressure affects rheumatism's develoment, especially since it varies continually day in and day out and hour by hour, but cooler and damper weather affects the frequency of Streptococcus pyogenes infections. Damp weather is usually connected with lower barometric pressure and cooler dry weather often is connected with clear, high-pressure weather patterns, in the winter. The fall through the late spring is generally cooler in the northern hemisphere.
It is a sure fact that high altitude areas such as the Rocky Mountain area in the USA has an elevated frequency for the development of rheumatic fever cases for it was proved during the WW II period. Rheumatic fever, acute rheumatism, and therefore the development of chronic rheumatism is not limited, however, to any particular altitude or climate.
The high-altitude area of Mexico features endemic rheumatic fever and I surely think that the great number of immigrants to the USA from Mexico, usually individuals from the more economically poor class, have been vectors for virulent strains of Streptococcus pyogenes and that great immigration phenomenon has probably been one of the causes of the increased level of rheumatism as indicated by the increased incidence of acute rheumatic fever in the USA since 1987, and therefore, the cause of the increase in the incidence of autism, diabetes, and other autoimmunological diseases in the USA during the last thirty years.
Miscellany
A Trod in the West of England is a straight line or Fairy Path in the grass of a field with a different shade of green to the rest. People with rheumatism sought relief by walking along these tracks, though animals are thought to avoid them.[1]
"For the period of 1939-1943, statistics published by the Metropolitan Life Insurance Company indicated that rheumatic fever was the leading cause of death among policy holders for persons from five to nineteen years of age and the second leading fatal disease among twenty to twenty-four year olds." Rheumatic Fever and Streptococcal Infection, cited above.
References
- ↑ Pennick, Nigel (1996). Celtic Sacred Landscapes. Thames & Hudson. ISBN 0-500-01666-6. P. 132.
External links
- BBC "Your Health" website on Arthritis and Rheumatism
- List of plant species that have been recommended as treatments for rheumatism, from Dr Duke's Phytochemical and Ethnobotanical Databases
- Account of Rheumatism from the website of Retirement Matters Ltd of the UK