Infectious Agents Of ‘Itch’- The Causative Factors Of Miasm Of ‘Psora’
According to samuel Hahnemann, the “miasm” of PSORA is the cause of a wide range of chronic diseases. He explained PSORA as the residual chronic effects of INFECTIOUS AGENTS OF ITCH.
If anybody has least doubt whether or not hahnemann was talking about the ‘miasm of psora’ as originating from ‘infection of itch disease’, kindly read this part from ‘Chronic Diseases’-Para 37:
“Psora (itch disease), like syphilis, is a miasmatic chronic disease, and its original development is similar. The itch disease is, however, also the most contagious of all chronic miasmata, far more infectious than the other two chronic miasmata, the venereal chancre disease and the figwart disease”.
“But the miasma of the itch needs only to touch the general skin, especially with tender children”.
“No other chronic miasma infects more generally, more surely, more easily and more absolutely than the miasma of itch; as already stated, it is the most contagious of all. It is communicated so easily, that even the physician, hurrying from one patient to another, in feeling the pulse has unconsciously inoculated other patients with it; wash which is washed with wash infected with the itch; new gloves which had been tried on by an itch patient, a strange lodging place, a strange towel used for drying oneself have communicated this tinder of contagion; yea, often a babe, when being born, is infected while passing through the organs of the mother, who may be infected (as is not infrequently the case) with this disease; or the babe receives this unlucky infection through the hand of the midwife, which has been infected by another parturient woman (or previously); or, again, a suckling may be infected by its nurse, or, while on her arm, by her caresses or the caresses of a strange person with unclean hands; not to mention the thousands of other possible ways in which things polluted with this invisible miasma may touch a man in the course of his life, and which often can in no way be anticipated or guarded against, so that men who have never been infected by the psora are the exception. We need not to hunt for the causes of infection in crowded hospitals, factories, prisons, or in orphan houses, or in the filthy huts of paupers; even in active life, in retirement, and in the rich classes, the itch creeps in.”
I think we have to study the INFECTIOUS AGENTS OF ITCH in detail, in order to understand the MIASM OF PSORA. Then only we can realize why Hahnemann considered PSORA as the mother of CHRONIC DISEASES
Scabies (from Latin: scabere, “to scratch”), known colloquially as the seven-year itch, is a contagious skin infection that occurs among humans and other animals. It is caused by a tiny and usually not directly visible parasite, the mite Sarcoptes scabiei, which burrows under the host’s skin, causing intense allergic itching. The infection in animals (caused by different but related mite species) is called sarcoptic mange.
The disease may be transmitted from objects but is most often transmitted by direct skin-to-skin contact, with a higher risk with prolonged contact. Initial infections require four to six weeks to become symptomatic. Reinfection, however, may manifest symptoms within as little as 24 hours. Because the symptoms are allergic, their delay in onset is often mirrored by a significant delay in relief after the parasites have been eradicated. Crusted scabies, formerly known as Norwegian scabies, is a more severe form of the infection often associated with immunosuppression.
The characteristic symptoms of a scabies infection include intense itching and superficial burrows. The burrow tracks are often linear, to the point that a neat “line” of four or more closely-placed and equally-developed mosquito-like “bites,” is almost diagnostic of the disease.
In the classic scenario, the itch is made worse by warmth and is usually experienced as being worse at night, possibly because there are fewer distractions. As a symptom it is less common in the elderly.
The superficial burrows of scabies usually occur in the area of the hands, feet, wrists, elbows, back, buttocks, and external genitals. The burrows are created by excavation of the adult mite in the epidermis.
In most people, the trails of the burrowing mites show as linear or s-shaped tracks in the skin, often accompanied by what appear as rows of small pimple-like mosquito, or insect bites. These signs are often found in crevices of the body, such as on the webs of fingers and toes, around the genital area, and under the breasts of women.
Symptoms typically appear 2–6 weeks after infestation for individuals never before exposed to scabies. For those having been previously exposed, the symptoms can appear within several days after infestation. However, it is not unknown for symptoms to appear after several months or years. Acropustulosis, or blisters and pustules on the palms and soles of the feet, are characteristic symptoms of scabies in infants.
The elderly and people with an impaired immune system, such as HIV and cancer sufferers or transplant patients on immunosuppressive drugs, are susceptible to crusted scabies (formerly called “Norwegian scabies”). On those with a weaker immune system, the host becomes a more fertile breeding ground for the mites, which spread over the host’s body, except the face. Sufferers of crusted scabies exhibit scaly rashes, slight itching, and thick crusts of skin that contain thousands of mites. Such areas make eradication of mites particularly difficult, as the crusts protect the mites from topical miticides, necessitating prolonged treatment of these areas.
In the 18th century, Italian biologist Diacinto Cestoni (1637–1718) described the mite now called Sarcoptes scabiei, variety hominis, as the cause of scabies. Sarcoptes is a genus of skin parasites and part of the larger family of mites collectively known as “scab mites”. These organisms have 8 legs as adults, and are placed in the same phylogenetic class (Arachnida) as spiders and ticks.
Sarcoptes scabiei are microscopic, but sometimes are visible as pinpoints of white. Pregnant females tunnel into the stratum corneum of a host’s skin and deposit eggs in the burrows. The eggs hatch into larvae in 3–10 days. These young mites move about on the skin and molt into a “nymphal” stage, before maturing as adults, which live 3–4 weeks in the host’s skin. Males roam on top of the skin, occasionally burrowing into the skin. In general, there are usually few mites on a healthy hygienic person infested with non-crusted scabies; approximately 11 females in burrows can be found on such a person.
The movement of mites within and on the skin produces an intense itch, which has the characteristics of a delayed cell-mediated inflammatory response to allergens. IgE antibodies are present in the serum and the site of infection, which react to multiple protein allergens the body of the mite. Some of these cross-react to allergens from house-dust mites. Immediate antibody-mediated allergic reactions (wheals) have been elicited in infected persons, but not in healthy persons; immediate hypersensitivity of this type is thought to explain the observed far more rapid allergic skin response to reinfection seen in persons having been previously infected (especially having been infected within the previous year or two). Because the host develops the symptoms as a reaction to the mites’ presence over time, there is usually a 4– to 6-week incubation period after the onset of infestation. As noted, those previously infected with scabies and cured may exhibit the symptoms of a new infection in a much shorter period, as little as 1–4 days.
Scabies is contagious, and can be spread by scratching an infected area, thereby picking up the mites under the fingernails, or through physical contact with a scabies-infected person for a prolonged period of time. Scabies is usually transmitted by direct skin-to-skin physical contact. It can also be spread through contact with other objects, such as clothing, bedding, furniture, or surfaces with which a person infected with scabies might have come in contact, but these are uncommon ways to transmit scabies. Scabies mites can survive without a human host for 24 to 36 hours. As with lice, scabies can be transmitted through sexual intercourse even if a latex condom is used, because it is transmitted from skin-to-skin at sites other than sex organs.
The symptoms are caused by an allergic reaction of the host’s body to mite proteins, though exactly which proteins remains a topic of study. The mite proteins are also present from the gut, in mite feces, which are deposited under the skin. The allergic reaction is both of the delayed (cell-mediated) and immediate (antibody-mediated) type, and involves IgE (antibodies, it is presumed, mediate the very rapid symptoms on re-infection). The allergy-type symptoms (itching) continue for some days, and even several weeks, after all mites are killed. New lesions may appear for a few days after mites are eradicated. Nodular lesions from scabies may continue to be symptomatic for weeks after the mites have been killed.
Scabies may be diagnosed clinically in geographical areas where it is common when diffuse itching presents along with either lesions in two typical spots or there is itchiness of another household member. The classical sign of scabies is the burrows made by the mites within the skin. To detect the burrow the suspected area is rubbed with ink from a fountain pen or a topical tetracycline solution, which glows under a special light. The skin is then wiped with an alcohol pad. If the person is infected with scabies, the characteristic zigzag or “S” pattern of the burrow will appear across the skin; however, interpreting this test may be difficult, as the burrows are scarce and may be obscured by scratch marks. A definitive diagnosis is made by finding either the scabies mites or their eggs and fecal pellets. Searches for these signs involve either scraping a suspected area, mounting the sample in potassium hydroxide, and examining it under a microscope, or using dermoscopy to examine the skin directly.
Symptoms of early scabies infestation mirror other skin diseases, including dermatitis, syphilis, various urticaria-related syndromes, allergic reactions, and other ectoparasites such as lice and fleas.
Mass treatment programs that use topical permethrin or oral ivermectin have been effective in reducing the prevalence of scabies in a number of populations. There is no vaccine available for scabies. The simultaneous treatment of all close contacts is recommended, even if they show no symptoms of infection (asymptomatic), to reduce rates of recurrence. Asymptomatic infection is relatively common. Objects in the environment pose little risk of transmission except in the case of crusted scabies, thus cleaning is of little importance. Rooms used by those with crusted scabies require thorough cleaning.
A number of medications are effective in treating scabies, however treatment must often involve the entire household or community to prevent re-infection. Options to improve itchiness include antihistamines.
Scabies is one of the three most common skin disorders in children along with tinea and pyoderma. The mites are distributed around the world and equally infects all ages, races, and socioeconomic classes in different climates. Scabies is more often seen in crowded areas with unhygienic living conditions. Globally as of 2009, it is estimated that 300 million cases of scabies occur each year, although various parties claim the figure is either over- or underestimated. There are one million cases of scabies in the United States annually. About 1–10% of the global population is estimated to be infected with scabies, but in certain populations, the infection rate may be as high as 50–80%.[Scabies is one of the three most common dermatological disorders in children.
Scabies is an ancient disease. Archeological evidence from Egypt and the Middle East suggests that scabies was present as early as 494 BC. The first recorded reference to scabies is believed to be from the Bible (Leviticus, the third book of Moses) ca. 1200 BC. Later in fourth century BC, the ancient Greek philosopher Aristotle reported on “lice” that “escape from little pimples if they are pricked”; scholars believe this was actually a reference to scabies.
Nevertheless, it was Roman physician Celsus who is credited with naming the disease “scabies” and describing its characteristic features. The parasitic etiology of scabies was later documented by the Italian physician Giovanni Cosimo Bonomo (1663–99 AD) in his famous 1687 letter, “Observations concerning the fleshworms of the human body.” With this (disputed) discovery, scabies became one of the first diseases with a known cause.
Scabies may occur in a number of domestic and wild animals; the mites that cause these infestations are of different scabies subspecies. These subspecies can infest animals or humans that are not their usual hosts, but such infections do not last long. Scabies-infected animals suffer severe itching and secondary skin infections. They often lose weight and become frail.
The most frequently diagnosed form of scabies in domestic animals is sarcoptic mange, which is found on dogs. The scab mite Psoroptes is the mite responsible for mange. Scabies-infected domestic fowls suffer what is known as “scabies leg”. Domestic animals that have gone feral and have no veterinary care are frequently afflicted with scabies and a host of other ailments. Non-domestic animals have also been observed to suffer from scabies. Gorillas, for instance, are known to be susceptible to infection via contact with items used by humans.
Please listen to this:
“Archeological evidence from Egypt and the Middle East suggests that scabies was present as early as 494 BC. The first recorded reference to scabies is believed to be from the Bible (Leviticus, the third book of Moses) ca. 1200 BC.” Now we can understand why hahnemann said PSORA has been inherited through “GENERATIONS OF HUMANITY” up to our period. Even now most of us get infected with ITCH in early life, and ANTIBODIES are formed in our body, which is the exact material basis of all those diseases we consider of PSORIC MIASM
Please note this also:
“Globally as of 2009, it is estimated that 300 million cases of scabies occur each year, although various parties claim the figure is either over- or underestimated. There are one million cases of scabies in the United States annually. About 1–10% of the global population is estimated to be infected with scabies, but in certain populations, the infection rate may be as high as 50–80%.[Scabies is one of the three most common dermatological disorders in children”.Even now, in spite of all modern treatments and personal hygeine, this remains the most widespread disease affecting humanity. Imagine what would be the situation during hahnemann’s period. NO WONDER, HAHNEMANN CONSIDERED PSORA AS THE MOTHER OF CHRONIC DISEASES.
NOTE THIS POINT:
“The symptoms are caused by an allergic reaction of the host’s body to mite proteins, though exactly which proteins remains a topic of study”. As part of this allergic response of our body to “mite proteins”, antibodies are generated. “The allergic reaction is both of the delayed (cell-mediated) and immediate (antibody-mediated) type, and involves IgE (antibodies, it is presumed, mediate the very rapid symptoms on re-infection)”. These antibodies remain life long in our body as CHRONIC MIASMS. Antibodies can attack OFF-TARGET biological molecules in various biochemical channels in the body, resulting in diverse types of CHRONIC diseases belonging to MIASM OF PSORA.
Latest available studies states that the SCABIES MITES carries different species of BACTERIA on their wings and body, and the toxins secreted by these BACTERIA are the the real molecular factors that give rise to allergic reactions during MITE infections. If that is true, SCABIES or PSORA will have to ultimately considered as BACTERIAL INFECTIONS.
Antibodies are native globulin proteins ‘imprinted’ with exogenous protein molecules entering into the organism from the environment, as infections, food, drugs, toxins or as part of any interactions with the environment. These exogenous proteins may come from bacterial/viral/fungal/parasitic infections that invade the body, bites and stings of insects and serpents, uncooked food articles, drugs like antibiotics and serum, vaccines, and so on. These exogenous foreign proteins, alien to our genetic constitution, are dangerous to the normal functioning of the organism, and have to be destroyed or eradicated. Body has a well organized defense system for this, which we call immune system. Foreign proteins are called antigens. Body prepares immune bodies or antibodies against these dangerous invaders. Antibodies are specific to each antigen, There are also polyclonal antibodies, which can identify different antigens. Antibodies are exactly native proteins of globulin types, which have peculiar molecular structure with an active group known as ‘paratope’ on its periphery. Active groups of antigen molecules are known as ‘epitopes’. Epitopes of antigens and paratopes of antibodies has a ‘key-lock’ relationship of configuration. They should fit exactly each other in order to happen an immune reaction. Paratopes of antibodies once interacted with epitopes of a particular antigen undergoes a process of ‘molecular imprinting’, by which the ‘memory’ of epitope is imprinted into the paratope of antibody. Even after the antigens are destroyed and eradicated by the immune system, these ‘molecular imprinted’ globulins, or antibodies exist and circulate in the organism, in most cases life long. This is the mechanism by which life long immunity is attained through certan infections and vaccinations. These antibodies, or ‘molecular imprinted proteins’ are very important part of our defense system, playing a vital role in protecting us against infections.
Same time, these ‘molecular imprinted proteins’ or antibodies plays a negative role also, which is what we call ‘miasms’. They can act as pathogenic factors. Whenever these antibodies happen to come in contact with a native biological molecule having a structural group of configuration similar to the ‘epitope’ of its natural antigen, its paratope binds to it and inhibits the biological molecules. This is a ‘molecular error’ amounting to a state of pathology. Diverse types of chronic diseases and dispositions are created by the antibodies in the organism. These pathological conditions caused by ‘off-target’ binding of antibodies or ‘molecular imprinted proteins’ are the real ‘miasms’ hahnemann described as the underlying factors of ‘chronic diseases’.
Obviously, identifying and removal of these ‘off-target’ molecular blocks or ‘miasms’ caused by antibodies or ‘molecular imprinted proteins’ is an important part in the treatment of chronic diseases. Observing and collecting the whole history of infections and intoxications that might have generated antibodies are important in the management of chronic diseases. History of skin infections, venereal infections, stings of poisonous creatures, vaccinations, serum/antibiotic treatments, sensitization with protein foods etc. has to be collected in detail and appropriate ‘anti-miasmatics’ included in the treatment protocols of chronic treatments.
Another important thing we have to remember is that we cannot permanently inactivate ‘antibodies’ using potentized nosodes or anti-miasmatic drugs. Our drugs may act in two ways. If the nosodes are prepared from antibodies themselves, they contain ‘molecular imprints of epitopes of ‘exogenous toxins’ or antigens themselves. These ‘molecular imprints can compete with the paratopes of antibodies in binding to biological molecues, and prevent them from creating ‘off-target’ biological blocks. Since ‘molecular imprints’ cannot successfully compete with the epitopes of antigens in binding with the paratopes of antibodies, our potentized drugs never interferes with the normal immune mechanism of the body. They only prevents antibodies from binding to ‘off-target’ biological molecules, and thus act as ‘antimiasmatics’.
If we are preparing nosodes by potentizing antibodies themselves, our drugs contains ‘molecular imprints’ of paratopes of antibodies. These molecular imprints can bind to the paratopes, thereby preventing them from interacting with ‘off-target’ biological molecules. Same time, they also cannot interfere in the interaction between antibodies and their natural antigens, which have comparatively increased affinity. In any way, potentized nosodes or ‘antimiasmatics’ will not weaken the normal immunological mechanism of the organism.
Since we cannot eradicate or permanently inactivate antibodies or miasms with our potentized drugs, we have to administer antimiasmatic drugs in frequent intervals, probably life long. This is a very important realization evolving from the understanding of ‘miasms’ as ‘antibodies’ or ‘molecular imprinted proteins’.
I think hahnemann included all ‘itch’ producing infections under the carpet of ‘psora’. He mentioned about Leprosy, scarlet fever, scabies and many such ‘infectious’ agents as causative factors of psora. He talked about “three miasms”, only because those three infectious agents were creating havoc in europe during his period. According to me, this classification of psora, syphilis and sycosis is not much relevant if we understand ‘miasms’ in terms of ‘antibodies’.
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