The Tubercular Constitution as a Common Cause of Chronic Diseases and its Treatment with Naturopathic “Regulation Therapy”
von
Peter Schneider
Copyright © 2000 by Peter Schneider
It's much easier to ride the horse in the direction he's going --- Werner Erhard
Content
Historical background of the tubercular constitution
Homotoxicology according to Reckeweg
Characterisation of the tubercular milieu
Naturopathic regulatory treatment of the tubercular constitution
Historical background of the tubercular constitution
Almost 200 years ago, Samuel Hahnemann (Hahnemann, 1810, 1828) tried to classify chronic disease into certain “miasms” (disease energies). He attributed the basic toxic load to Psora (in Greek “the itch”), to Syphilis and to Sycosis (“fig-wart disease”). This work dates from the latter part of his life.
Even in ancient cultures it was recognised that all the chronic diseases that afflict mankind form a unified whole. Escaping from his opponents to Paris at the age of 80, Hahnemann tried to secure this knowledge in the 6th edition of his “Organon of the Rational Art of Healing” by adding a number of notes to the 5th edition. Due to the fierce opposition of some medical doctors to the notion of Psora, the 6th edition was only published in 1921. In that way the fanatically contested idea of Psora, which Hahnemann called the “thousand headed monster of disease” and which was dismissed as a senile fantasy of his, was handed down in its original form.
Among Hahnemann’s numerous followers John H. Allen deserves mention, for his intensive work on the theory of the miasms. (Allen, 1996). Hahnemann and his pupils had already observed that suppressive treatment of disease would intensify and increase the miasmatic disease energies. It was further realised that, when inherited, Psora and Syphilis may completely merge together. The tubercular constitution is a “mixed” miasm and a result of this merging together. Allen calls it “absolutely the strongest of all disease states or conditions”. It can be inherited or acquired and is also called “pseudo-psora”.
As the tubercular constitution does not signify a case of clinical tuberculosis, other terms such as “para-tuberculosis”, “tuberculinic” or “tubercular miasm” were introduced later. However, the term “para-tuberculosis” is nowadays used internationally, in a different sense, to denote an illness caused by Mycobacterium paratuberculosis (Johne’s disease in cattle).
Between 55 and 100 years ago clinical tuberculosis was widespread, and intensive research on it was carried out. In Berlin, Germany, Robert Koch pioneered the diagnosis and treatment (Tuberculinum Koch) of tuberculosis. His assistant Carl Spengler carried on his work and based his new methods of diagnosis and treatment of chronic illness on Koch’s findings (Spengler, 1911). Above all, Spengler’s work was concerned with the different morphology of strains of mycobacteria (“dualism”) and with the close relationship between tubercle bacteria and the pathogenic agent of syphilis, whose bacterial form is found in mixed cultures from tuberculosis patients. Spengler showed that the presence of the syphilis pathogen can be demonstrated within the cells of an organism in an ultra-small and primitive variety - even when an infection by this pathogen had never occurred during the individual’s life-time.
It was assumed that the general spread of “inherited syphilis” stems from the beginning of the 16th century, when a whole population was infected with a syphilis pandemic “imported” from America. Anyone who did not die of this infectious disease at that time, retained a residual toxicity in the body that was passed on through generations and, according to Spengler, would later show up as an “inherited virus”.
Spengler developed the so called “Spengler colloids” which were named after him and are antigens from different bacteria and anti-toxins produced from the blood of highly immunised rabbits. With the help of these substances it is possible to diagnose various chronic diseases such as the “inherited toxins” of tuberculosis and syphilis (see POLYSANS, produced by the SANUM-KEHLBECK Co).
In a study on trans-placental carcinogenesis in mice, an extra-chromosomally transmitted susceptibility to tumour growth could be observed (Schneider, 1981). In the F2-generation only those animals showed an increased occurrence of tumours, whose parent of the same sex had been transplacentally exposed to the chemical carcinogen (DMBA) and had been crossed with a non-treated animal. This dependency on the sex and trans-placental exposure regarding tumour formation permits the assumption that extra-chromosomal influences are at work.
By the end of the last century the French chemist and pharmacist Antoine Béchamp had claimed (Béchamp, 1912), that certain micro-organisms could occur in various forms and stages of development. Under exactly defined conditions they would occur, ranging from the lowest forms to the highly developed stages of bacteria and fungi. He found that all animal and plant cells contain minute granules (“microzymas”), which do not perish after the death of an organism, are responsible for fermentation, and from which other micro-organisms could also develop. These microzymas would be present in every living species, in humans, animals and plants; they were eternal and indestructible and represented a bridge between non-living and living matter. Under certain or pathogenic influences these microzymas could develop into bacteria with putrefacient and fermenting properties. This meant that disease had its origin mainly within the body.
In the year 1997 Stanley Prusiner won the Nobel Price "for his discovery of prions - a new biological principle of infection". These prions are probably nothing else than the micozymas which were discovered by Béchamp about 100 years earlier.
Claude Bernard, a French physiologist and a contemporary of Béchamp, confirmed his results and found out in addition that not only the micro-organisms themselves are harmful, but primarily the “soil” in which they multiply.
Another contemporary of theirs at the end of the nineteenth century was Louis Pasteur. He claimed that the explanations of Béchamp and Bernard were arrant nonsense. He contested these views in accord with the botanist Cohn (Breslau) and Robert Koch’s theory of “monomorphism” (meaning that each type of bacteria is only allowed one mode of growth and manifestation). His opinion prevailed among the experts of his time and still does so even in modern times. Nevertheless Pasteur said on his death bed: “Bernard is right; the soil is everything, the microbe nothing”. Pasteur’s private notes about his scientific research were kept secret from the general scientific community at his request. Not until 1975 were 10,000 pages of his laboratory protocols handed over to the historian G. L. Geison at Princeton University, who spent almost 20 years evaluating them. In 1993 Geison handed over his results to the American Association for the Advancement of Science in Boston. In 1997 a book containing Geison’s findings was published. (Geison, 1997). This book shows Pasteur’s merits, but does not cover up the fact that that he manipulated some of his experimental results and contravened medical, scientific and ethical rules.
Fontes (Fontes, 1910) who had based his research on Spengler’s results, delivered important proof of the “pleomorphism” of bacteria. He was the first to provide proof of the infectiousness of bacteria-free filtrates of TBC-bacterial cultures. As a result of his research Fontes assumed that not only the predisposition to tuberculosis could be inherited, but also the virus in its “filterable”, granular form. He further thought that the latter could remain latent (“latent tuberculosis”) or could develop slowly into the classic bacterial type.
G. Enderlein (zoologist and microbiologist, curator of the zoological museum of Berlin University, and microbiologist for the German army in Stettin during World War I) reported in 1916 for the “Friends of Natural Research”, Berlin, about his time as a bacteriologist in the army and his research results regarding the development of bacteria. Owing to the prevailing conditions resulting from the war, his monograph on this subject was only published in 1925 (Enderlein, 1925). As he was describing morphological facts that had previously been unknown to microbiology, he developed a whole new terminology; however, this resulted in the procedures he described being difficult to understand.
According to Enderlein, microbes pass through a cycle which is specific to their species. The term “cyclogeny” describes the changes and the journey of pathogenic and non-pathogenic micro-organisms through all phases (“valencies”). The cycle starts below the limits of microscopic visibility, the viral sphere, then on via forms of higher valency like cocci and bacilli, to culminate in the fungal phases. The bacterial nucleus (“mych”) has a special significance. Although this was already known before Enderlein, its function had not been interpreted accurately. According to the “basic Anatartic Law” fomulated by Enderlein, the increase in valency of the microbe depends on the “milieu” that is present in blood and tissues, which is mainly characterised by its pH value. Bacteria can either multiply asexually by division or branching (“auxanogeny”) or sexually after prior fusion of cell nuclei (“probænogeny”). Sexual multiplication is essential for movement to a higher or lower phase. 40 years after Enderlein’s discovery, the Nobel prize was awarded to Lederberg in 1958 for discovery of “polymorphy” and sexual multiplication of bacteria by the fusion of cell nuclei (Lederberg, 1958).
Apart from naming the various phases in the development of micro-organisms, Enderlein also succeeded in proving the existence of the most important symbiont (“endobiont”) in warm-blooded creatures. He discovered Mucor racemosus Fresen(ius) 1870, in all its developmental stages from viral to fungal. In the low valency stages, the endobiont lives as a physiological regulator; in the higher valency stages it will develop pathogenic characteristics, depending on the environment (or milieu) that surrounds it. Changes in the environment which are followed by an endobiosis occur in all chronic illnesses. The endobiosis caused by Mucor racemosus in a higher-valency form is characterised by congestive symptoms (e.g. diseases of the blood and venous system, wounds, hearing loss and neurodermatitis).
Enderlein also found that the pathogenic higher-valency phases of the endobiont could be reconverted into a non-pathogenic phase by introducing low-valency forms while simultaneously treating the milieu (“isopathic therapy”). These processes can be observed with the help of dark-field microscopy of vital blood. (Schwerdtle and Arnoul, 1993; Bleker, 1997).
According to Enderlein, viruses are cell-free primitive forms (“filum”) of the endobiont, from which bacteria may be grown. (For example: the tobacco mosaic virus, from which it was possible to breed bacteria after several months); bacteriophages however are “spermits” of the microbes (Enderlein, 1954).
The causative agent of the second electively pathogenic endobiosis which, in contrast to the Mucor symbiosis, is non-physiological, was identified by Enderlein as the mould Aspergillus niger van Tieghem. In its polymorphy and phase-dependent pathology this is believed to be a causative agent of cancer (Dechow, 1933) and tuberculosis. Vaudremer (1921) and Tissot (1925) had already found a genetic connection between the tubercle bacillus and fungi of the species Aspergillus (according to Enderlein, 1949).
The cyclode of Aspergillus niger, according to Enderlein, is a scission from the cyclode of Mucor racemosus (Figure 1).

Figure 1: Hypothetical separation of the Aspergillus niger cyclode from that of Mucor racemosus
(Arnoul, 1998; Rau, 1998)[The cyclogenies of Mucor racemosus and Aspergillus niger
Bakterie = bacterium
Mucor-Zyklode = Mucor cyclode
Aspergillus-Zyklode = Aspergillus cyclode
Pathogene Phase = pathogenic phase
Apathogene Phase = non-pathogenic phase
Abbau zur Urform = deconstruction back to the original form]
According to Enderlein, the low valency phases of Mucor racemosus and Aspergillus niger are transmitted via the placenta.
The higher and high valency phases of Aspergillus are closely connected with calcium metabolism and cell respiration (citric acid cycle) and they cause chronic tubercular diseases in warm blooded creatures “to the right of the biological incision” (Reckeweg, table 1). Examples are chronically relapsing susceptibility to infections, tuberculosis, paratuberculosis, asthma, arthrosis, ankylosing spondylitis, cysts, ovarian and prostate diseases, as well as cancer. Among the tubercular symptoms degenerative diseases such as auto-immune disorders may also be found.
The particular significance of high-valency fungal forms in the development of neoplastic disorders was confirmed by Privy Councillor Prof. Dr. F. Gerlach, Director of the Bundesanstalt für Tierseuchenbekämpfung (National Institute for the control of epidemics among animals) in Mödling near Vienna, following detailed research. Gerlach was able to culture fungi from cancerous material of human or animal origin (including chemically induced tumours from animal testing) at every attempt (Gerlach, 1948). Later he also found that mycoplasma play an important role in carcinogenesis. From this it may be assumed that mycoplasma which, according to Mattman are barely distinguishable from CWD-types (see below), are higher valency forms of the Aspergillus-cyclode.
Tubercular diseases were given various names by Enderlein’s contemporaries, without acknowledging any connection to the bacterial cycle. Scrophula, lymphatism, camouflaged tuberculosis (Patromikolas), masked tuberculosis (Willy Bircher), certain forms of rheumatic disease (Poncet), latentia, tubercular toxicosis, paratuberculosis. "Much’s Granules" and "Spengler’s splinters" also belong in this category.
The “Basit”, “Linit”, and “Ascit” stages of Aspergillus are the short and long bacilli of Sclerothrix tuberculosis Koch 1882, acidoresistant and non- acidoresistant, the cultivation of which was described by Enderlein in all its phases (Enderlein, 1959).
After Enderlein, Harmsen also described forms of Mycobacterium tuberculosis which deviated from the slender bacillary form: branched varieties, granula, acidoresistant and non-acidoresistant forms, mycelium formation, nuclear equivalents and vacuole formation (Harmsen, 1952).
Just as the low-valency phases of Mucor racemosus are especially suited to the treatment of endobiosis, so tubercular diseases can be treated very effectively isopathically with low valency phases of Aspergillus niger. According to Enderlein the Aspergillus-cyclode is an off-shoot from the Mucor-cyclode and therefore the medicine is also prescribed in a combination from both cyclodes.
An extensive survey of the numerous studies on polymorphic “symbionts”, particularly in German speaking countries, was carried out by Windstosser (Windstosser, 1995) .
In English-speaking countries too, intensive research on the pathogenicity of polymorphic forms of microbes has been carried out during the last 40 years. Probably because of the language barrier, the results of earlier research remained unnoticed. Only in recent times has an effort been made by Canadian research groups to pool this knowledge (First International Symposium on Pleomorphic Microbes in Health and Disease, 18th-19th June 1999, Montreal, Canada).
The existing investigations on the properties and pathogenicity of the so called “Cell Wall Deficient Forms” (CWD) were recently summarized by Lida H. Mattman, Emeritus Professor of Microbiology at Wayne State University, Detroit, Michigan (Mattman, 1993).
“CWD” is used as the umbrella term for synonyms like “L-forms”, “L-phases” or “spheroplasts” that can be found in the literature. CWD also covers the previously used term “protoplast”. Figure 2 shows cell wall deficient bacterial forms of the blood under a dark-field microscope. The elements with the thick, white peripheral zones are erythrocytes.

Figure 2: CWD ("Mychite") in vital blood under the dark-field
microscope
(from Bleker, 1997)
CWD have special characteristics that are not present in classical micro-organisms:
Destruction of many forms during fixation with heat;
they usually require soft agar, grow under the surface and need a mature, autoclaved culture medium;
they typically grow within erythrocytes;
they are often serophilic;
most types grow best in a hypertonic and alkaline environment (ph 7.8 – 8.0);
CWD are able to revert to classical bacterial forms.
It is only possible to culture CWD under special conditions. The culture medium has to be stabilised with an extract of heart muscle, 15% inactivated horse serum and 3.5% sodium chloride.
The following are some examples of the intra-erythrocytal growth of CWD:
|
normal and physiological |
Staphylococci, Bacillus licheniformis (in approx. 30% of all healthy humans) |
|
Sarkoidosis |
Mykobacteria |
|
Kaposi's sarkoma |
Fungi |
|
Nephropathy |
Lysis of erythrocytes from 489 patients: the same species as in urinary infections |
|
Idiopathic hæmaturia |
Bacteria similar to streptococci; in contrast to this, children with nephrotic syndrome exhibited an elevated staphylococcal growth-rate |
|
Systemic lupus erythematosus |
Bacteria connected with nephrotic diseases |
|
Crohn’s disease |
Pseudomonas, mycobacteria |
|
Auto-immune diseases |
CWD act as haptens and stimulate the formation of haemolytic antibodies (Example: paroxysmal hæmoglobinuria due to cold in syphilitics) |
The formation of pathogenic CWD from bacteria can be induced by suppressive treatment. in-vitro their formation is possible through antibiotics, e.g.:
|
Penicillins |
Inhibition of murein synthesis: Brucella, Clostridia, E. coli, Haemophilus influenzae, Listeria monocytogenes, Proteus mirabilis, Salmonella gallinarum, S. typhi, Vibrio cholerae, Vitreoscilla. |
|
Streptomycin |
Mycobacteria (e.g. Mycobacterium tuberculosis and Mycobacterium paratuberculosis) |
|
Sulfonamides |
Staph. aureus |
|
Kanamycin, |
Inhibition of protein synthesis, resulting in surface changes in bacteria: E. coli, Klebsiella pneumoniae, Bacillus megaterium, B. polymyxa, Serratia marcescens, Sarcina lutea, Staphylococcus aureus, Salmonellen, Shigellen, Proteus |
|
Aztoreonam |
(Monobactam) surface changes in E. coli |
|
Erythromycin |
Staphylococcus aureus (and at least 40 other macrolid-antibiotics such as Leukomycin, Oleandomycin, Spiramycin, Tylosin) |
|
Tetracyclines |
Staph. aureus, E. coli, K. pneumoniae, B. megaterium, B. polymyxa, Serratia marcescens, Serratia lutea, Salmonellæ, Shigellæ, Proteus |
As an example of an in vivo induction of CWD by antibiotics Mattman names antibiotic treatment of mastitis in cows caused by Staphylococcus aureus:
- apart from the classical bacterial forms, the CWD of Streptococcus agalactiae, Staphylococcus aureus and Corynebacterium pyogenes were also demonstrated as causative of bovine mastitis (Bergmann and Böckel, 1989).
- following treatment of mastitis caused by Staphylococcus aureus with Cloxacillin the excretion of classical forms of cocci ceased within a few days, whereas CWD forms of Staph. aureus continued to contaminate the milk for more then 30 days (Sears, P.M. et al., 1987).
Nowadays the induction of pathogenic CWD in vivo by using antibiotics is of great importance as antibiotic-resistant micro-organisms are widespread and can no longer necessarily be destroyed (Beyer, 1999). On the other hand CWD commonly escape from the immune system due to their lack of a cell wall and continue to act as haptens. To support the organism in the elimination of cell wall deficient microbial forms, the SANUM-therapy which includes SANUKEHL preparations should be the treatment of choice. (Schneider, 1999a; Werthmann, 1999).
On the basis of clinical research to date it can reliably be asserted that:
Micro-organisms can be of a polymorphic phenotype, from the smallest viral structures to bacteria and fungi.
CWD of micro-organisms (staphylococci and bacilli) appear physiologically in the erythrocytes of healthy humans.
Cell wall deficient forms can occur in vitro and in vivo under certain environmental or “milieu” conditions and can be pathogenic in vivo.
CWD pathogenic forms can live as parasites within erythrocytes and can be observed in vital blood under a dark-field microscope.
Suppressive treatment of disease, especially with antibiotics, can induce the development of CWD.
Cell wall deficient forms of mycobacteria are the real carriers of a tubercular constitution.
CWD are able to revert to classical forms of bacteria. According to Enderlein they can move through their cyclodes in both directions.
Pathogenic forms of micro-organisms can be rendered harmless when transformed into their non-pathogenic regulatory forms.
Homotoxicology according to Reckeweg
According to Reckeweg (Reckeweg 1975, 1980) the body’s “major defence system” consists of 5 different mechanisms (reticulo-endothelium, anterior pituitary-NNR-mechanism, nerve reflexes, liver detoxification, detoxifying function of connective tissues) by which the body defends itself against toxins (“homotoxins”), which can otherwise bring about illness. Either the body wins in this fight and gets damaged in varying degrees by the homotoxins or it succumbs to the toxic effects.
These views of Reckeweg’s are an extension of Selye’s research on the Adaptation Syndrome (Selye, 1953).
The damage caused by the homotoxins manifests in the form of an impairment or blockage of the intracellular enzyme systems. In Reckeweg’s system, the different grades of toxic effects are expressed as six different phases. During the first three phases (excretion, reaction, deposition) the excretion of toxins is successful, whereas during the three cellular phases that lie beyond the “biological incision” (impregnation, degeneration, neoplasm) the cells are increasingly damaged and become more or less non-functional. The three cellular phases often result from the suppression of acute illnesses. Numerous chemically defined substances such as antibiotics, anti-rheumatic drugs, analgesics, bacteriostatics among others, according to Reckeweg often have an irreversible blocking effect on the intracellular fermentation systems and bring the cellular phases four to six into play (“progressive vicariation”). These phases correspond to the terms “psora” and “sycosis” which were originated by Hahnemann, or with the “tubercular constitution”. According to Reckeweg’s six-phase scheme (table 1), clinical tuberculosis only appears in the degeneration phase.
The following authentic case example will serve to clarify the term “progressive vicariation”. The patient is a young male whose medical history began in infancy as a “dysbiosis” with an acute, inflammatory, excretory reaction and developed over 16 years into a degenerative demyelinisation of the central nervous system:
|
Age |
Disease |
Treatment |
|
2 months |
Pre-toxicosis with Coli-Dyspepsia, diffuse peri-bronchitis, high fever |
antibiotics i.v.and i.m., milk-based “health-food”, fluoride |
|
4 months |
Super-infected varicella, anal fissures, streptococcal sepsis, high fever |
antibiotics, antipyretics, |
|
5 months |
Coli-dyspepsia, chickenpox, diarrhœa, vomiting |
antibiotics, immuno-globulins, |
|
1 year |
superinfected intertriginous eczema,
eczema of scalp, infection of lungs
(mild), |
antibiotics, antifungals, |
|
14 months |
histiocytosis X, constipation |
chemotherapy, prednisolone |
|
2 years |
histiocytose X, recurrent focal of infection on right side |
chemotherapy, corticoids |
|
6 years |
accident |
tetanus vaccination |
|
7 years |
loss of teeth after chemotherapy |
|
|
14 years |
Cerebellar ataxia, hydrocephalus int., anal fistula, kyphoskoliosis, dwarfism, anus præter, mental and motor retardation |
valve implant owing to hydrocephalus |
|
16 years |
increasing muscular dystrophy, nystagmus, astigmatism, demyelination in pons and und mesenzephalon, strabism, unable to walk after steriotactic biopsies, patient confined to a wheelchair |
further attempts at corticoid treatment; aborted after onset of Cushing’s syndrome and aggravation of acne |
According to Reckeweg the aim of a biological therapy is to enhance detoxification and excretion via the major defence mechanism. The reactivation of the damaged or blocked enzyme systems by administering adequate co-factors such as vitamins, trace elements, intermediate citric acid cycle catalysts and quinones is of the utmost importance. A biological therapy also aims to transform the “dangerous” phases on the right side of the biological incision into less harmful phases (“regressive vicariation”). An example is the induction of inflammatory reactions in neoplasma phases.
Reckeweg concludes that all natural healing operates according to the principle of regressive vicariation. The individual phases of the pathogenesis are briefly re-experienced in the reverse order of their appearance, beginning with the most recent events. This means that during recovery apparently new illnesses seem to appear (e.g. appearance of acute herpes during the treatment of a degenerative disease). Under no circumstances must these symptoms be suppressed. In such cases relief can be obtained by intensifying the use of excretory measures, by giving a classical homœopathic remedy that is indicated for a certain stage of illness, or by acupuncture.
Table 1: Homotoxicosis: 6-phase Table, after Reckeweg, 1975
Tissue
Humoral Phases
Diseases of DISPOSITION
B
i
o
l
o
g
i
c
a
l
i
n
c
i
s
i
o
nCellular (tuberculinic) phases
Diseases of CONSTITUTION
Excretion
Reaction
Deposition
Impregnation
Degeneration
Neoplasma
Ectoderm
Saliva
Dermatitis
Warts,
PolypiMigraine,
LeucoplakiaChronic
dermatitisBasalioma
Nasal
catarrhRhinitis
Atheroma
Multiple
sclerosis,
EpilepsyLupus,
PsoriasisAdenoma
Sweat
Furuncle
Cataracta
senilisAsthma,
Hay feverCushing’s
syndromeMelanoma
Tears
Stomatitis
Incipient
asthmaRhinitis
atrophicansM.S.,
Parkinson’sSarcoma
Herpes
zoster,
NeuralgiaUlcus
ventric./duod.Menière’s,
Alzheimer
Entoderm
Intestinal
juicesColitis
syndromeConstipation
Asthma
Tuberculosis
Carcinoma
of pancreas,
gall bladder,
intestines
Bile
Enteritis
Megacolon
Ulcus
ventric./duod.Diabetes
mellitusMyeloma
Pancreatic
juiceParotitis
Struma
Recurrent
infectionsCirrhosis
of liverSarcoma
Hepatitis
Silicosis
Chronic
tonsillitis
Cholangitis
Cholelithiasis
Mesenchym
Antibody
productionOedema
Adiposity
Lymphatism
Tuberculosis
Sarcoma and
carcinoma
of kidneys
Vicarious
bleedingAbscess,
UlcerGout
Elephantiasis
Scleroderma
Menstruation
Angina
Lymph node
swellingsIncipient
agranulo-cytosisFibroma
Sarcoma and
carcinoma of
serous
membranes
Typhus
Otosclerosis
Uterine
carcinoma
Appendicitis
Lipoma
Paradontosis
(final stage)Myosarcoma
Polyarthritis
Exostosis
Leukæmia,
Lymphoma
Mesoderm
Lactic acid
productionCystitis
Myogelosis
Hydro- nephrosis
Exhaustion
(Selye)Carcinoma of skin and genitals
Discharge
of serous membranesPyelitis
Myalgia
Prostages
of tumoursTuberculosis
Nephritis
Rheuma
Atrophic
kidney
Prostatitis
Cysts
Muscular
dystrophy
Salpingitis
Muscular rheumatism
Excretion principle; prognosis favourable
Condensation principle; prognosis doubtful
Characterisation of the tubercular milieu
By “the milieu of the tissues” we mean the “cell milieu system”, whose properties have been described by Pischinger (Pischinger, 1990).
Changes in the milieu can be characterised on various levels, for instance by dark-field microscopy or on an electromagnetic level with the aid of Vincent’s system of Bio-electronics (BEV).
In the dark-field microscopy hæmogram of native blood changes may be observed in the morphological structure of erythrocytes related to their position on the right side of the “biological incision”. The observations extend from changes in the shape of erythrocytes to forms similar to a “thorn apple” (see Figure 3; Schwerdtle and Arnoul, 1993; Bleker, 1997). These structures have been described, documented and named by Enderlein and they can easily be reproduced. For dark-field microscopy exami