Sandbox Turky3

Parminder

Mohamad Alkateb, MBBCh [1]

The development of a rheumatic fever episode depends on the involved host being highly autoimmunologically sensitized to autoantigens exhibited by Streptococcus pyogenes to its host during prior Streptococcus pyogenes infectious episodes, so a decrease in the frequency and virulence of infections by Streptococcus pyogenes in a society can cause rheumatic fever, as a disease entity, to be less frequent and less severe.

Rheumatic fever affects individuals who are thought to be "young and healthy", for instance, individuals between four years and fifty years of age, but during most eras rheumatic fever was most commonly noted in individuals between the six and thirty. The reason children younger than four years of age, or so, do not usually develop rheumatic fever is that an individual must have sufficient, prior stimulation by Streptococcus pyogens autoantigens, which is, typically, caused by multiple infections by Streptococcus pyogenes, over a relatively short period of time, and that situation is less likely to occur in younger children (although it does happen!). Older individuals are expected, somewhat, to develop diseases of aging and so it is often not surprising when they become sick; it is surprising when individuals in their teens, twenties, thirties, forties and even fifties, for instance, become very sick so those cases attract more "medical" attention. Individuals of all ages, however, can develop rheumatic fever.

Scarlet fever and rheumatic fever are, primarily, the same disease. The somewhat typical rash of scarlet fever develops if an individual contracts an infecton from a strain of Streptococcus pyogenes that secretes erythrotoxin A, B, and C, and if the individual involved has not had an infection by that particular strain previously, since during a previous infection antibodies will have been developed against the erythrogenic toxin of interest. Repeated infections by strains of Streptococcus pyogenes that have, and do not have, erythrotoxin A, B, and C can reinforce each other in the development of autoimmunological reactions by a host, since they all have certain autoantigens and secreted toxic products, other than erythrotoxin A, B, and C, in commonk. If a person, usually a child, develops an infection from Streptococcus pyogenes that secretes A, B, or C erythrotixin they will develop a mild infectious/autoimmunological disease and the classic, mild rash of scarletina, the diminuative term for scarlet fever, will often develop.

Since the development of rheumatic fever depends upon a prior, high-level of autoimmunological stimulation, which itself depends upon an individual, in the past, experiencing many infectious episodes by Streptococcus pyogenes, and since Streptococcus pyogenes are endemic in human and domestic animal populations (information from the Russian Encyclopedia (V.Nasonova,E. Talahaev), it must be understood that all individuals experience pathological, autoimmunological stimulation during Streptococcus pyogenes infections.

The rate of development of rheumatic fever, in a somewhat homogeneous population, will depend upon the environmental conditions mentioned above, wherein crowding and unhygienic living conditions are two of the most important. Information in the text Streptococcal Infections (Stevens, D., Kaplan, E., Oxford University Press, 2000) indicate that 1% to 70% of individuals in various populations are carriers of Streptococcus pyogenes and many of them are asymptomatic carriers. Perhaps, 2% to 4% of individuals who contract Streptoccus pyogenes infections develop recognizable rheumatic fever (but most mild cases go unrecognized) and of those, a low percentage, about 1% to 3% die from rheumatic fever. The incidence of rheumatic fever depends, to a great degree, upon the general level of Streptococcal pyogenic, auto-immunological sensitivity that exists within members of a given population.

Contrary to the immunological protection developed by humans during most infections, infections by Streptococcus pyogenes cause both a protective immunological and a pathological autoimmunological stimulation and so repeated infections by Streptococcus pyogenes will cause both a heightened protective immune, and pathological autoimmune response. The immune response causes Streptococcus pyogenes to be controlled, but the concomitant, autoimmunological response causes an inflammatory, systemic, disease process to be developed within the affected individual. The systemic, inflammatory, autoimmunological disease process is termed rheumatic fever and it is a sequela of both the virulent, triggering Streptococcus pyogenes infection and the prior infections that the individual developed that caused them to have elevated auto-immunological sensitivity to Streptococcus pyogenes' autoantigens.

If an individual develops rheumatic fever, they will experience the development of increased sensitization to Streptococcus pyogenes auto-antigens. An infection by a virulent strain of Streptococcus pyogenes, at a later date, will likely cause an elevated, autoimmunological response and a recurrent case, probably a more severe case, of rheumatic fever will develop.

If an individual does not contract a Streptococcus pyogenes infection for a long period, perhaps for five years or longer, an individual's immunological/auto-immunological responsivness will naturally decrease and, perhaps, there will be less chance of developing rheumatic fever if the individual contracts a future Streptococcus pyogenes infection.

The above natural phenomenon is the basis for the use of prophylactic penicillin therapy for individuals, and populations of individuals, who are at risk for rheumatic fever. Providing individuals who have had rheumatic fever with monthly (or maybe every three weeks) injections of Benzathine Penicillin G, 1,200,000 units, or oral penicillin VK or G, 250mg twice daily (I think 500 mg twice daily is more efficacious), decreases the frequency of recurrent Streptococcus pyogenes infections and therefore recurrent rheumatic fever episodes. It is estimated that the recurrence rate of rheumatic fever is decreased about 85% by providing prophylactic penicillin therapy.

Streptococcus pyogenes is a complex microorganism and it causes many disease entities both from the suppurative aspect of Streptococcus pyogenes infections and from nonsuppurative, systemic, autoimmunological sequelae to the infections. The nonsuppurative, systemic, autoimmunological sequelae are inflammatory in nature and therefore all tissues and organs are affected, but certain organs are noted to be affected in an important and acute fashion: the heart, kidneys and brain.

Since the heart, kidneys and brain are vital organs, and their functional abnormalities causes obvious clinical abnormalities, and even death, to individuals, acute rheumatic abnormalities to the heart, kidneys and brain, that individuals experience, are medically-noted more frequently than acute rheumatic damage to other organs. The symptoms and signs of acute rheumatic fever, however, indicates that virtually all tissues, and therefore organs, of the body are affected: connective tissue (arthritis); lethargy, stupor, seizures, coma, post-disease fatigue, tics, chorea, chronic mental disturbances such as obsessive-compulsive behavior and PANDAS(rheumatic encephalomyelitis); acute rheumatic myocarditis,endocarditis, pericarditis and cardiac arrhythmias with the myocarditis and endocarditis causing cardiac failure and pulmonary edema (the heart); autoimmune pneumonitis (the lungs); rheumatic, vasculitic renal failure (kidneys); erythema marginatum, papulatum, miliary rash, purpura, petechiae, and scarlet fever rash (the skin); anemia, including aplastic anemia (bone marrow); autoimmune hepatitis (the liver); acute, peripheral, painful neuropathies (peripheral nerves); nausea, vomiting, diarrhea, crampy abdominal pain (gastrointestinal organs); other organs such as the pancreas, endocrine organs, and elements of the circulatory system are also affected. Since rheumatic fever is, basically and initially, an autoimmune inflammatory disorder, and the autoimmunological elements travel throughout the body via the circulatory system. Vascular elements, arteries, arterioles, capillaries, venules, veins and lymph vessels are attracked initially and in that way rheuamtic fever becomes a systemic disease process.

Information in modern texts has emphasized for many decades the affect of rheumatic fever on the heart, because its inflammatory, autoimmunological effects are exacerbated in that organ, and since the heart is a vital organ the clinical ramifications are easily noted. The reason that rheumatic autoimmunity is exacerbated in the heart's tissues is because the cyclic, physiological compression developed by the heart also causes an elevated vascular triple response of Lewis phenomenon within the heart's tissues. The triple response of Lewis phenomenon is usually thought to be a dermatological concept since it can be elicited by stroking the skin of most individuals. Those who have elevated Streptococcus pyogenic autoimmunity exhibit a very high-grade triple response of Lewis phenomenon dermatologically. Surpisingly, the triple response of Lewis phenomenon that all people exhibit indicates that all people have, at least, a low-level of rheuamtic autoimmunity (from personal research).

Major criteria

• Carditis: inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
• Migratory polyarthritis: a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
• Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease.
• Erythema marginatum: a long lasting rash that begins on the trunk or arms as macules and spread outward to form a snakelike ring while clearing in the middle. This rash never starts on the face and is made worse with heat.
• Subcutaneous nodules (a form of Aschoff bodies): painless, firm collections of collagen fibers on the back of the wrist, the outside elbow, and the front of the knees. These now occur infrequently.

Minor criteria

• Fever: temperature elevation
• Arthralgia: Joint pain without swelling
• Laboratory abnormalities: increased Erythrocyte sedimentation rate, increased C reactive protein, leukocytosis
• Electrocardiogram abnormalities: a prolonged PR interval
• Evidence of Group A Strep infection: positive culture for Group A Strep, elevated or rising Antistreptolysin O titre
• Previous rheumatic fever or inactive heart disease

Other signs and symptoms

• Abdominal pain
• Nosebleeds
• Neurological pain such as lumbago or low back pain
• Delirium, stupor, seizures, coma
• Renal failure
• Pulmonary edema
• Ruddiness of the skin secondary to rheumatic vasculitis
• Ruddiness and swelling of the face and neck secondary to jugular system congestion itself secondary to rheumatic carditis and acute, congestive heart failure
• Rheumatic pneumonitis causing a congestive lung condition

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• Hepatitis

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