2M Livro Trevor Douglas

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DOUGLAS BLOOD
MICROSCOPY CENTRE
18 Kingswood Crescent, Lockleys, South Australia, 5032
Mobile Telephone: 0427860035
Email: training@drtrev.com
DARK FIELD LIVE BLOOD

MICROSCOPY
-dark field & beyond
Notes compiled by:

Dr. Trevor Douglas BSc(hons)PhD DipIAN FCMA
Nutritional Biochemist & Naturopath
Copyright; These notes remain the intellectual property of Dr. Trevor Douglas and are not to be
copied or reproduced in any way without the express permission of the author (2009).
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Index:
Title Page
I. Live Blood Microscopy 7
II. Dark Field Live Blood Analysis 10
III. The Blood 11
IV. Constituents of the Blood 11
1. Formed Elements 11
a. Red Blood cells 12
b. The White Blood Cells 14
i. Granular Leucocytes 14
(1) Neutrophils 15
(2) Eosinophils 16
(3) Basophils 16
ii. Agranular Leucocytes 17
(1) Lymphocytes 18
(2) Monocytes 18
(3) Macrophages 18
(4) Plasma cells 19
2. Thrombocytes 20
3. The Plasma 21
4. The Serum 21
V. Blood cell Formation 21
1. Red Blood Cell Production 23
2. White Blood cell Production 23
3. Platelet Production 24
VI. Blood Disorders 24
1. Anaemia 24
a. Nutritional Anaemia 26
b. Pernicious Anaemia 26
c. Sickle Cell Anaemia 26
d. Haemorrhagic Anaemia 27
e. Haemolytic Anaemia 27
f. Aplastic Anaemia 27
g. Thallacaemia 28
2. Infectious Mononucleosis 28
3. Parasites 28
a. Malaria 28
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b. Trypanosomiasis 29
c. Spiroketes 29
4. Thrombocytopenia 29
5. Thrombocytosis 29
6. Haemophilia 29
7. Scepticaemia 29
8. Fungaemia 30
9. Other 30
VII. The History of the Theory of Disease 30
VIII. Pleomorphism 35
1. History 35
2. Pleomorphism vs Monomorphism 50
a. The Germ Theory 50
b. The Cellular Theory 50
IX. Controversies in Live Blood Analysis 51
1. Where do Microorganisms in the Blood Originate? 51
2. Do Candida spp. exist in the Blood of “Healthy” individuals? 53
X. Dark Field Live Blood Microscopy 54
1. Blood Collection 55
2. Microscopy 56
3. Observations and Recommendations 57
a. Normal, “Healthy” Blood 57
i. Erythrocytes 57
ii. Neutrophils 58
iii. Eosinophils 58
iv. Basophils 59
v. Monocytes 59
vi. Lymphocytes 60
vii. Phagocytic Macrophages 60
viii. Platelets 61
b. Abnormal Red Blood Cell Observations 62
i. Protein Linkage 62
ii. Rouleaux 63
iii. Erythrocyte Aggregation 64
iv. Anisocytosis 65
(1). Microcytes 65
(2) Macrocytes 65
v. Poikilocytosis 66
(1) Pencil Cells 67
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(2) Elliptocytes 68
(3). Acanthocytes 68
(4) Spiked/Crenated/Shadowed RBC’s/Echinocytes 69
(5) Hypochromic Cells 70
vi. Red Blood Cell Inclusion Bodies 70
vii. Red Blood cell Patterns, Crescents 71
viii Target Cells. 72
ix. Spherocytes 72
x. Schistocytes, Bite cells 73
c. Abnormal White Blood Cell Observations 73
i. White Blood cells Fewer than Normal 73
ii. White Blood cells More than Normal 74
iii. Neutrophils Too Few, Granules Inactive 74
iv. Neutrophils Hypersegmented 75
71 Neutrophils Irregular, Fragile 76
v. Eosinophils Excessive 76
vi. Basophils Excessive 76
vii. Lymphocytes Excessive 77
viii. Lymphocytes Too Few 77
ix. Enlarged T-Cells 77
x. Monocytes Excessive 78
xi. Macrophages Excessive 78
xii. Band Neutrophils 78
xiii. Blasts 78
d. Abnormal Platelet Observations 79
i. Platelet Aggregation 79
ii. Platelets Surrounded by Mucopolysaccaride 80
e. Other Observations 80
i. Fats and Fibrin 80
(1).Chylomicrons Excessive 80
(2) Fibrin Net 81
(3) Lipid Ribbons 82
(4) Protoplasts 82
(5) Atherosclerotic Plaque 83
ii. Crystals 83
(1) Cholesterol Crystals 83
(2) Uric Acid Crystals 84
(3) Red Pseudocrystals 85
(4) Orange Pseudocrystals 86
(5) Blue Pseudocrystals 86
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iii.Microbial Observations 87
(1) L-Forms 87
(2) Mycoplasmas 88
(3) Bacterial Forms 90
(a) Coccal Forms 90
(b) Rod Forms 90
(c) Spirochetes 91
(4) Yeast Buds 92
(5) Mycelial Forms 93
(6) Black Fungus 93
(7) Aspergillus Drepanids 94
(8) Aspergillus Symplasts 95
(9) Mucor Symplasts 96
XI. Pleomorphic Organisms 96
1. Enderlein’s Endobiont Theory 97
a. Enderlein’s Pleomorphic bodies in the blood 97
Bacteriophages and Spermits 100
2. Naessen’s Somatide Cycle 106
X. Microbes in Peripheral Blood – A Modern Perspective 108

1. Shapes of Microorganisms 108
2. Relative Size of Microorganisms in the Blood 109
3. L-Forms of Bacteria 110
4. Mycoplasmas 112
5. Leptotrichia buccalis 113
6. Pathogenic ‘Fungi’/Moulds 114
a. Moulds 114
b. Yeasts 114
7. Moulds and Fungi in Peripheral Blood 114
8. pH, Oxygen & Growth of Microorganisms 115
9. Acid-Base Balance – The Milieu 115
10. Enderlein’s Pleomorphic Cyclode Updated 119
11. Glossary of Enderlein Terms 119
XIII. Isopathy and Sanum Therapy 121

1. The 3 Cyclogenies (Cycles) 122
a. Mucor racemosus Cyclode 122
Mucor racemosus Forms Found in Live Blood 123
b. Aspergillus niger Cyclode 129
Aspergillus niger Forms Found in Live Blood 129
c. Penicillium Cyclode 132
Penicillium Forms Found in Live Blood 132
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2. Isopathy and Disease 137

3. Chronicity of a Complaint 138
4. Organic Acid Specificity of Fungi 138
5. The 4 Steps to Sanum Therapy 138
6. Blockages (Mochloses) 141
7. Prescribing Sanum 146
Sanum Flow Chart (Australia) 146
8. The 7 Steps to Restoring Health to the Individual 153
XIV. Categories of DFLBM Observations 155

XV. Microbial Indications from the Blood 156
XVI. DFLBM Overview 157
XVII. DFLBM Morphological Drawings 158
XVIII. DFLBM Observations and Possible Indications 173
XIX. Live Blood Microscopy References 177
Food for Thought:
“the mind is like a parachute – it only works when it is open” Anon
I would like to start by quoting from Dr. Robert Becker’s book “The Body Electric” (9) in
which he sums up some of the quandaries that we face as health practitioners and how modern
day medicine has strayed from the path of compassion and open mindedness to one of a narrow
minded ‘scientific’ drug related approach to healing directed by the Phamaceutical companies.
He states that “There is only one health, but diseases are many. Likewise, there appears to be
one fundamental force that heals, although the myriad schools of medicine all have their
favourite ways of cajoling it into action. Our prevailing mythology denies the existence of any
such generalized force in favour of thousands of little ones sitting on pharmacists’ shelves,
each one potent against only a few ailments or even a part of one.”
… most medical systems have combined such specifics with a direct, unitary appeal to the
same vital principle in all illnesses. The inner force can be tapped in many ways, but all are
variations of four main, overlapping patterns: faith healing, magic healing, psychic healing,
and spontaneous healing. Although science derides all four, they seem to work as well for
degenerative diseases and long-term healing as most of what Western medicine can offer.”
He further states that “Real science is creative, as much as painting, sculpture, or writing.
Beauty, variously defined, is the criterion for art, and likewise a good theory has the elegance,
proportion, and simplicity that we find beautiful. Just as the skilled artist omits the extraneous
and directs our attention to a unifying concept, so the scientist strives to find a relatively
simple order underlying the apparent chaos of perception.”
The main thrust of all health treatments must, first and foremost, have the welfare of the
patient in mind and be aimed at returning the patient to a state of health and well-being. In
many cases disease states can be prevented by careful thought and good advice from the health
practitioner concerning the patient’s general nutritional intake and lifestyle. If a patient
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becomes ill then these same factors must be addressed along with any prescribed isopathics,
homeopathics, herbs, nutritional supplements, or even drugs, in order to allow the patient to
regain, and maintain, a good state of health. Live Blood Microscopy is designed to allow the
practitioner to screen and, by interaction and feedback from the patient, ascertain the patient’s
health status (not disease state) and, based on those findings, design an individualized
treatment protocol to assist the patient in returning to a state of health. As Dr. Robert Bradford
once stated:
“Any fool can diagnose disease but it takes a good doctor to diagnose health. Let’s hope that
more health practitioners can become good doctors”
I. LIVE BLOOD MICROSCOPY - HISTORY:
Live Blood Microscopy is often called Live Blood Analysis which is just a generic term to
describe the morphologic examination and evaluation of peripheral blood using dark field,
phase contrast, and differential interference microscopy. Its origins were attributed, primarily,
to Prof. Antoine Béchamp who, during the mid 19th century, used dark field microscopy to
examine blood while it was still ‘alive’.
Dr. Günther Enderlein, a contemporary of Béchamp, carried out extensive dark field
examination of live blood and confirmed what Béchamp had discovered plus much more.
Enderlein continued to study dark field microscopy of microbes in blood until his death in1968
but his theories and cyclogenies of microbes were first published in 1925. His protits are most
probably equivalent to Béchamp’s microzymas because they are the same size (around 0.01µ
diameter), they are invisible under normal dark field microscopy and they have a similar action
in the body. Protits can become visible when present in very large quantities in the blood in
which case they form a ‘protit veil’. Other dark field microscopists who also discovered similar
(or identical) forms as Béchamp’s microzymas included Gaston Naessens (somatids) and Reich
(bions). More recently, Dr. Phillipa Uwins, at the University of Queensland, used electron
microscopy to identify living units smaller than the cell which she named nanobes (148) and
which may also be akin to Béchamp’s microzymas. Some also argue that Béchamp’s
micozymas may, in fact, be what Pasteur described as virus particles.
Béchamp studied the blood and a book on his works describing the blood elements and fibrin
and its role in the coagulation process was published just after his death (8). His work was
extended by Enderlein through the early 1900’s. In 1936, Hansen-Pruss also applied the use of
dark field microscopy to the clinical examination of peripheral blood and described many of
the blood cell elements in detail (70).
Through the 1970’s and 1980’s dark field microscopic examination of live blood was
established as a tool for the identification of parasitic microorganisms such as the causative
agent of syphilis, Trepanema pallidum (30) and oral bacteria associated with periodontic
abscesses (145, 117).
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In the late 1980’s Dr. Philip Hoekstra introduced the technique of Hemaview in combination
with the work of several other workers such as Hansen-Pruss, Hernan Acevedo, Anthony
Almada, Roderick Chiodini, and Gerald Domingue. Hemaview is a purely dark field
examination of the blood and all its elements. Hoekstra justified the use of this technique for
clinical assessment of patients by scientifically validating several observations and their
potential indications. There are still other observations in the blood, however, that he has been
unable to scientifically validate and yet are very real because they have clinical validity but just
have not yet been examined scientifically.
Also in the late 1980’s Dr. Robert Bradford (Bradford Research Institute) developed the
technique of Live Blood Analysis which he later named High Resolution Live Blood
Morphology (HRBM®) to differentiate it from purely dark field microscopy techniques.
Realising the short-comings of dark field microscopy, Bradford introduced the use of a
combination of dark field and phase contrast microscopy to give better identification of
crystals, certain microorganisms, platelets, and black bodies in the blood while developing
HRBM®. In the 1990’s he introduced the use of ‘psuedo’differential interference microscopy
to the HRBM® technique to further expand its capabilities. The scientific validation of
observations and their indications by dark field was extended to include phase contrast
microscopic observations. The ability to switch quickly between dark field and phase contrast
allowed the proper identification of microorganisms, blood cell types, and blood cell
inclusions, dispelling indications applied to of some of the earlier dark field observations and
adding to others.
All microscopy depends upon two main factors:
1. Resolution (the ability to differentiate two objects close together)

2. Contrast (the ability to observe objects clearly and distinctly against their background)
Bright field microscopy is most commonly used on dried, stained, blood smears but suffers
from the point that the cells are dead while being observed and the messy use of stains. It is,
however, very useful as a pathology tool. Sometimes (especially with live blood preparations)
it is impossible to stain the specimen. Further, resolution in bright field illumination is limited
to 3µ so it is unsuitable for live blood examination. For these reasons dark field analysis was
used extensively for live blood analysis until the advent of phase contrast.
Dark field works on the basis that objects are observed from scattered light with no direct light
entering the condenser of the microscope. The human eye is sensitive only to brightness and
colour so dark field is good because it produces a bright object against a black background
which intensifies contrast. Even though it is far superior to bright field for examining live
blood, dark field is unable to allow the observer to view black bodies (objects that do not
refract light but rather absorb it). In this case, a black object is viewed against a black
background so is invisible to the observer. Certain microorganisms fall into this category.
Further, because dark field employs very high light intensity to illuminate the object, many
highly crystalline objects (including specks of dust that may be on the microscope slide even
after scrupulously cleaning) literally glow under dark field and their basic structure is lost or
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poorly defined. Dark field is best for observing the outer structure of objects (borders, outlines,
and edges) but is less useful in revealing internal structures unless those structures are highly
refractive.
Phase contrast overcomes the shortcomings of dark field and offers good resolution and
identification of objects not visible under dark field. In phase contrast (developed by Zernike to
observe the process of mitosis in living cells) the object can appear either as a dark object
against a bright background (positive contrast) which is suitable for observing the internal
structure of cells and nuclei) or negative contrast which is suitable for the observation of low
contrast objects. To improve contrast using phase, filters (usually green or blue) are used. The
only down side of phase contrast is that it exhibits a ‘halo’ effect of incident light around 3-
dimensional objects such as red blood cells. It is not a major drawback but can be overcome by
using differential interference.
Differential Interference microscopy is a more recent technique developed entirely for the
examination of low contrast objects such as living cells and their internal components. It
provides the observer with a 3-D view of objects. The method uses filters and modified prisms
instead of phase annuli and retardation rings and eliminates the ‘halo’ effect seen around the
perimeter of cells viewed under phase contrast (1, 2). With the “pseudo” differential
interference technique it is possible to get a usable differential interference pattern.
By combining dark field, phase contrast, and “pseudo” differential interference microscopic
examination we get the best of all three techniques and the most powerful and most
comprehensive live blood analysis available (the Live Blood Morphology [LBM] test).
The purpose of this course, however, is to introduce you to, or extend your knowledge of,
live blood microscopy using only dark field examination (DFLBM).
Acknowledgement: The author would like to thank the generosity of David Woolcott and Ian
Flay, naturopaths, and Dr. Thomas Rau from Paraselsus Clinic, Switzerland who, as friends
and colleagues, have providing some of the photographs of the blood that are presented in
these notes. Without their generosity there would have been a few gaps in the presentation.
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II. DARK FIELD LIVE BLOOD MICROSCOPY
Dark Field Live Blood Microscopy (DFLBM), as presented here, is a technique based largely on
orthodox haematology, Drs. Robert Bradford and Henry Allen’s HRBM® blood microscopy test,
Hemaview, Dr.Michael Coyle‘s Live Blood Analysis, scientific publications, some of my own
clinical observations, and additionally embraces some of the findings of scientists and medical
researchers who have not been endorsed by the scientific community but who’s theories are worthy
of consideration in regard to live blood examination. These individuals include Antoine Béchamp,
Gaston Naessens, Günther Enderlein, Royal Raymond Rife, Emanuel Ravici, and many others who
arrived at very different conclusions about the cause of disease which conflict with the Pasteur Germ
Theory being the only theory of disease, and consequently were discarded by the medical fraternity.
Where information could not be validated either scientifically or clinically it has been discarded.
DFLBM is a powerful screening technique that works well and is becoming increasingly accepted
by naturopaths and open-minded medical practitioners alike. A study of the morphology of blood
cells, other elements in the blood, and blood physiology is essential in order that we understand how
interpretive data flowing on from this knowledge is ascertained. The DFLBM test is a microscopic
examination of living blood cells and other blood elements in which observed deviations from
‘normal’ morphology (shape, size, colour, activity etc.) are interpreted according to what we know
regarding how these morphological changes correlate with body burden (toxins, chemicals,
microorganisms, physiological and pathophysiological functions etc) and body stresses (both
physical and emotional). The more proficient a practitioner is in their powers of observation and
questioning, the better they will become in assessing a patient for their health status. Once we
understand and establish the underlying causes of a patient’s health problem a specific treatment
protocol to assist the patient in regaining and maintaining health and well-being can be designed by
the practitioner.
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III. THE BLOOD

Blood is a red, viscous, solution which makes up approximately 8% of the total body weight. It is
exceptionally important to the health and well-being of every cell in the body:
1. The blood transports nutrients from the gastrointestinal tract, oxygen from the lungs, and
hormones from endocrine glands to all the cells in our body to support growth,
differentiation, respiration, and cell membrane integrity. It also transports carbon dioxide,
waste products, heat, and toxins away from the cells for elimination.
2. The blood also regulates pH through buffers (eg. bicarbonate), helps maintain normal body
temperature by virtue of the heat dissipating properties of water, regulates water balance
and ion concentration in the cells, maintains ideal gas and solute concentrations, and helps
regulate and maintain ideal body fluid pressure ie. The blood maintains homeostasis in our
bodies. If homeostasis is disturbed in any way our health can suffer and we may become
quite ill.
3. The blood has protective properties such as immune system action against microbes and
allergens through the action of certain phagocytic white blood cells and the production of
proteins such as antibodies, interferon, and complement. The blood also protects us against
blood loss through the coagulation pathways involving fibrin and platelets.
The importance of the blood is, therefore, obvious. It nourishes, protects, and detoxifies every cell
in every organ in the entire body! It is for these reasons that the blood offers us a perfect medium
with which to work if we want to find out the current status of health of the individual.
Deficiencies in the status of certain vitamins and minerals and the presence of waste products and
toxins can be easily determined. Red and white blood cells undergo specific changes in their
morphology (shape, size, mobility, etc.) in response to allergens, and changes in the mineral, and
vitamin balance in the body. Free radical activity damages red blood cell membranes leaving
specific 'fingerprints' in the blood which can be determined by live blood microscopy.
Any changes from ideal conditions (homeostasis) such as pH, temperature, solute concentration,
blood gas concentration, plasma specific gravity, ion concentration, cell membrane lipid
composition, and blood pressure can lead to ill health and will be reflected by morphological
changes in the blood cells, and other elements, in the blood. If homeostasis is not re-established it
can result in ill health and if left unchecked may eventually lead to death.
IV. CONSTITUENTS OF BLOOD

1. Formed Elements
The blood consists of red blood cells, white blood cells, and platelets suspended in a viscous fluid
called the plasma. These cells are known as the formed elements of the blood and constitute
approximately 45% of total blood volume.
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The red blood cells are called erythrocytes and there are around 5 million of these cells per cubic
millimetre of blood so they constitute, by far, the main formed elements of blood.
White blood cells (leucocytes) are present at around 5,000 to 10,000 per cubic millimetre and they
consist of neutrophils, eosinophils, basophils, lymphocytes, and monocytes.
Thrombocytes (platelets) are present in the blood at around 250,000 to 400,000 per cubic millimetre.
The number of each type of blood cell element in the blood is critical to good health and significant
variations in the numbers of any of the elements is indicative of health problems and even disease
states. For example, excessive numbers of red cells in the blood is known as polycythemia or
erythrocytosis and this may be observed in patients with cyanotic heart disease, thrombosis,
blockages of the microvasculature of lungs and kidneys, and in smokers. Low red cell numbers are
associated with anaemia and are also seen in patients undergoing radiation or chemotherapy for
cancers and in end-stage renal disease patients. Increases in the number of white blood cells, in
blood, is almost always indicative of an infection but can also be associated with inflammatory
conditions and certain types of leukemia.
It is important to remember that in healthy individuals all of the blood cell elements are ‘normal’,
mature, cells. The presence of immature (blasts) or ‘abnormal’ cells in the blood is indicative of a
deviation from a healthy state or even a disease state so the observation of live peripheral blood is
an excellent means of determining the health status of an individual. The presence of small numbers
of immature or abnormal cells in the blood may also be indicative of pre-disease states so the
DFLBM test can also provide the practitioner with a means of very early detection of a potential
health problem. The Dark Field Live Blood Microscopy test is a very subjective test which relies
heavily on feed-back from the patient. It is not a diagnostic test. Every change from ‘normal’
morphology observed in the blood may indicate more than one potential causative factor and it is
only by discussing the possible indications with the patient that the practitioner can arrive at the
correct conclusions as to what underlying cause(s) may be attributing to the patient’s health
problem(s). It is the feed-back from the patient that allows a diagnosis.
a. The Red Blood Cells
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Mammalian red blood cells are enucleate (no nucleus), biconcave, cells averaging around 7.5 - 8µ
in diameter, 2µ in width and contain, principally, haemoglobin. The biconcave shape of the red
blood cells is the geometric shape which has the greatest surface area of all known shapes so it
assists the red blood cell in absorption of the greatest possible amount of oxygen for transport
around the circulatory system. Haemoglobin is a molecule made up of four porphyrin protein rings
attached to four central iron moieties known as heme. It is the heme which gives the erythrocytes
their red colour. Iron in heme is able to complex with oxygen (forming oxyhaemoglobin) and carbon
dioxide (forming carbaminohaemoglobin) and it is this characteristic which gives red blood cells
their major function. Oxygen from the lungs is bound to haemoglobin in red blood cells (four
molecules of oxygen per haemoglobin molecule) and is carried to all cells in the body which, in
turn, use it for respiration (in their mitochondria). Carbon dioxide produced by these cells is then
bound to the heme and carried back to the lungs where it is expelled. About 23% of the carbon
dioxide from respiration is transported in this manner; the majority (about 70%) is transported in
the blood plasma as bicarbonate ions which confer the buffering capacity on the blood.
The red blood cells have an average life expectancy of about 120 days after which macrophages in
the spleen, liver, and bone marrow remove damaged, aged, red blood cells to rejuvenate the blood.
Haemoglobin from these old cells is broken down to iron (which associates with a protein to form
hemosiderin), bilirubin, and globin. The iron is reformed into haemoglobin in newly manufactured
cells in the bone marrow or stored as hemosiderin, bilirubin is secreted by the liver into bile, and
globin is metabolised by the liver to form amino acids for future protein synthesis in cells.
Red blood cell membranes are a typical phospholipid bilayer consisting of cholesterol (up to 30%
of the neutral lipid content), phospholipids (up to 40%), glycolipids, protein (up to 50%) and
carbohydrate (around 10%). Internal proteins are of a contractile nature and include spectrin, actin,
protein 4.1, and ankyrin. These proteins are responsible for the biconcave shape of the red blood
cells. Defects in these proteins and variations in the amount of certain lipids in the membrane will
alter the shape of red blood cells. For example, excess cholesterol will lead to the production of
acanthocytes (see later), increases in phospholipids and cholesterol content will lead to production
of target cells, defects in (or decreases in) spectrin proteins will produce spherocytes, and defects in
spectrin-dimer formation will lead to elliptocytosis. Variations in the normal, biconcave shape, of
red blood cells (poikilocytosis) and size (anisocytosis) are indicative of a number of physiological
and pathophysiological health states.
Reduced glutathione is a major player in the protection of red cell membranes from oxidative
damage through oxidative stress. Other antioxidants (vitamins A, C, E, sulfurophane etc),
germanium and selenium also play a significant role.
b. The White Blood Cells
White blood cells consist of approximately 60 - 70% neutrophils, 20 - 30% lymphocytes, 2 - 4%

eosinophils, 3 - 8% monocytes, and 0.5 - 1% basophils. These relative proportions will change
due to immune system activation through infections or allergy reactions. Typically, during an
infection the lymphocyte numbers will be significantly increased, and during an allergic reaction
eosinophil and basophil numbers will increase. Enderlein never made any distinction between the
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various types of white blood cells, calling monocytes leucocytes and neutrophils both leucocytes
and lymphocytes and, in fact, may have incorrectly attributed the granules inside some of the
granular leucocytes to being microbes (endobiont).
i. Granular Leucocytes
The granular leucocytes are so called due to the presence of granular deposits in their cytoplasm
making them quite distinct under microscopic examination. There are a number of different granular
leucocytes, all of which carry out different functions in the body. Most common are the neutrophils
which make up around 60 – 70% of all white blood cells. These, together with the eosinophils (2 –
4%) and basophils (0.5 – 1%), make up the range of granular leucocytes. Lymphocytes and
monocytes make up the rest of the leucocytes.
(1).Neutrophils
Neutrophils are also known as polymorphonuclear leucocytes (PMN’s) due to their several-lobed
nuclei. They are primarily involved in the phagocytosis of, or antibody production against, invading
organisms such as microbes (bacteria, viruses, fungi, mycoplasmas) and necrotic tissues produced
in the body due to wear and tear. Neutrophils are capable of ingesting the invading organisms
through phagocytosis (surrounding and then lysing the organisms with powerful enzymes such as
lysozyme). After ingestion the waste products and debris are disposed of via the lymphatic system.
Antibodies produced by neutrophils will protect the body against future infections. Generally, the
neutrophils have a short life-time varying from a few hours to a few days. About half of the
neutrophils we produce will circulate in the blood while the other half attach to the blood vessel
walls. During infection the neutrophils move rapidly into the infected area phagocytose the infecting
organisms, die, and are, themselves phagocytosed by macrophages. Neutrophils are usually the first
cells to enter an infected site and are our first line of attack by the immune system. Monocytes
follow shortly after the neutrophils as a second line of attack.
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(2). Eosinophils
Eosinophils are distinctly recognised from neutrophils by two main features viz. the presence of
dense granules in the cytoplasm; and only a two-lobed nucleus. They are able to release anti-
histamine compounds which counter the effects of histamines on the body. They leave the
capillaries and move into the extra cellular fluid where they phagocytose antigen-antibody
complexes produced as a result of an allergic reaction. Eosinophils are predominantly involved in
food and chemical allergies. They also are effective in combating parasitic infections so a high
eosinophil count in the blood is often an indication of either allergies or parasitic infections.
Elevated eosinophil numbers are also common to asthma sufferers. Eosinophils are armed with
binding sites for both IgG and IgE immunoglobulins as well as complement proteins. They are
specifically designed to destroy cells coated with IgG, IgE, and complement and live predominantly
in the skin and the airways (bronchi and bronchioles of the lungs) where they release chemicals that
damage foreign organisms. Possible indications of elevated eosinophil numbers include allergies
(143), damage to endocardium and microvasculature of the heart (50), and respiratory problems
associated with destruction of ciliated cells in the respiratory tract epithelium (57).
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(3). Basophils
Basophils are the least common of the granulocytes and exhibit chemotaxis and some phagocytic
activity. They release heparin in areas of foreign body invasion to prevent blood clotting at the site
to assist the passage of neutrophils and monocytes to the site of infection. They also release
histamine to bring about dilation of the pores of blood cells and thus assist with the passage of other
white blood cells across the wall of the blood vessels into the tissues of the body. Basophils may
also be involved in allergic reactions but appear to be more closely allied with environmental
allergies. Basophils also leave the capillaries and enter the extracellular fluid where they proceed to
release histamine, seretonin, and heparin. These substances actually intensify allergy reactions by
increasing inflammatory processes and are involved in hypersensitivity to allergens.
ii. Agranular Leucocytes
Agranular leucocytes have a cytoplasm free of granular deposits and include the Lymphocytes (T-
cells and B-cells), Monocytes, and Macrophages. Under certain conditions (eg. invading antigens)
B-cells can be converted into plasma cells that play a role in defending the body through their high
rate of production of an antibody to the antigen. Macrophages stimulate B-cells to produce plasma
cells through their production and secretion of interleukin-1. There are a number of different T-cells
such as killer T-cells, memory T-cells, helper T-cells, suppressor T-cells, and amplifier T-cells, all
of which play a significant role in how our immune system defends us from invading micro-
organisms.
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(1).Lymphocytes
Lymphocytes are involved in the production of antibodies which are special proteins, each of which
is totally specific for each individual antigen that invades the body. Antigens may be specific plant
proteins (pollens, grasses, etc.), chemical agents, or toxins released from bacteria which have
infected the body. Upon invasion of the body with an antigen one type of lymphocytes, the B-cells,
are converted to Plasma cells which, in turn, manufacture antibodies to specifically counter the
antigen. Antibodies bind with the antigens rendering them inactive. Further, antibodies have the
ability to actually destroy invading bacteria. After the antibody-antigen response is completed cells
called Phagocytes (Neutrophils and Macrophages) ingest and, thereby, destroy the antibody-antigen
complexes.
The other lymphocytes (the T-cells) include an array of cells which are intricately involved in
immune system activity, and specifically where viral infections occur.
Helper cells, killer cells, memory cells, and suppressor cells are all T-cells which have specific roles
in immune reactions. After the phagocytes (above) have reacted against invading viruses and
produced antibodies to them, they send an alert to the Helper T-cells which become activated and
begin to multiply. Activated T-cells also become enlarged and are easily distinguished from 'normal'
sized T-cells under the microscope. The activated Helper T-cells then summon up the Killer T-cells
which puncture the cell membranes of infected cells thus disrupting the replication cycle of the
viruses. B-cells then produce large numbers of antibodies to the virus which both neutralise and kill
the infecting virus particles. After the battle has been won, Suppressor T-cells signal for the close
of T-cell activation and Memory T-cells and B-cells are left in our bodies to rapidly recognise and
destroy any future invasion of the same virus (immunity).
One virus which is not successfully destroyed by the immune system is HIV (Human Immuno
Virus). This virus actually invades Helper T-cells, destroying them while using their DNA and
cytoplasmic contents to replicate themselves. T-cell numbers in HIV positive people are
accordingly very low. Thus Aids sufferers lose the very cells their bodies require to fight the virus.
The life span of white blood cells is very dependent upon the state of health of the individual as
these cells are continuously phagocytosing bacteria, viruses, and debris so are, in turn, being broken
18
down through antibody-antigen interactions. During a cold or flu, the life expectancy of white cells
may be as little as a few hours while in a very healthy individual it could be as much as a few
months. Generally, however, white blood cells survive for just a few days due to the constant
presence of bacteria in the pores of our skin and on mucous membranes in the nose, throat, and
mouth.
(2).Monocytes
Monocytes are more effective than lymphocytes in destroying bacteria as they arrive at sites of
infection in greater numbers where they carry out a phagocytic role. Monocytes are unique in that
they are basically immature cells that eventually differentiate into wandering macrophages which
are very efficient at cleaning up microbes and cellular debris. Macrophages are the ‘Pac-Men’ of
the circulating blood.
Monocytes are approximately 14 - 19 µ in diameter and are characterised by a single large nucleus
which is a kidney to U shape.
(3). Macrophages
The photo shown (below) is taken using phase contrast microscopy but under dark field they look
much the same. Sometimes they possess a few up to several vacuoles in the cytoplasm and
frequently they contain dark bodies which are mainly debris that they have consumed and are
digesting (phagocytosing). In this photo you can also see an inactive neutrophil to the left of the
macrophage.
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The macrophages are scattered throughout the body but are predominantly present in the sinusoids
of the liver, spleen, and lungs where they may reside for years to attack antigens which invade the
body. They also circulate through the lymphatic system where they act as antigen-presenting cells
which introduce fragments of antigen proteins to the T-lymphocytes for recognition and destruction
of invading anitigens and viruses. Macrophages produce and secrete interleukin-1 which stimulates
B-cells to enlarge, divide, and differentiate into plasma cells. Macrophages are a vital and integral
part of the immune system.
(4). Plasma cells
This photo is also in phase contrast but the essential size, shape, etc is the same under dark field.
Plasma cells are formed from B-cells under conditions of allergic reaction to environmental and
chemical allergens.
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iii. Thrombocytes
The blood platelets, or thrombocytes, are round or oval-shaped, enucleated, discs which average
from 2 - 4µ in diameter. Platelets are involved principally in the initiation of the clotting of blood at
the site of cuts and abrasions. In a normal healthy state the blood remains free of all coagulation
(clotting) and is free-flowing. In situations where there is a low level of essential omega-3 fatty
acids in the diet, an increase in platelet aggregation factor can occur and this may lead to platelet
aggregation in situ. Further lack of intake of these fatty acids may initiate premature blood clotting,
or thrombosis. Other factors involved with clotting include calcium, prothrombin, thromboplastin,
and a number of other coagulation factors but there are just three major stages in the clotting process.
These are:
a. formation of prothrombin activator.
b. conversion of prothrombin into thrombin.
c. conversion of soluble fibrinogen into insoluble fibrin which forms the threads which net together
with platelets to form a clot.
Prevention of blood clotting in individuals who have a propensity for thrombosis is usually
accomplished medically by administration of either heparin or warfarin. Heparin is produced by
mast cells and basophils and acts by removing thrombin in combination with antithrombin III
proteins in the blood.
Warfarin (the active ingredient of certain rat poisons) acts by inhibiting vitamin K activity thus
lowering prothrombin levels. Excess warfarin (as administered to rats) can lead to internal
hemorrhaging and subsequent death.
A lack of platelets will lead to chronic tiredness as is common in diseases such as lupus.
Platelets have a very short life span of some 9 to 12 days.
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2. The Plasma
The plasma, which constitutes approximately 55% of total blood volume, is made up mainly of
water (91.5%) with some dissolved solutes (1.5%) and proteins. The proteins are principally
albumins (55%), globulins (38%) and fibrinogen (7%). Solutes include nutrients (from digested
foods), nitrogeneous substances (urea, uric acid, amino acids, creatine, creatinine, ammonium salts,
etc.), respiratory gases (oxygen and carbon dioxide), electrolytes (sodium, potassium, chloride,
calcium, magnesium, sulphate, phosphate, etc.) and regulatory substances such as enzymes, co-
enzymes, and hormones.
Albumins, produced by the liver, are largely responsible for the viscosity of the blood. Globulins
are the group of proteins to which antibodies belong - these are produced by plasma cells.
Fibrinogen is intricately involved in the blood-clotting process along with thrombocytes. Fibrinogen
is produced by the liver. If the liver is under stress (excess work load due to the accumulation of
toxins in the blood) it will produce excess amounts of fibrin which is easily visualised in live blood
viewed microscopically.
The plasma carries the bicarbonate ions which are so important in the protective buffering role of
the blood.
3. The Serum
The blood serum consists of all the plasma components minus its clotting proteins (fibrinogen).
V. BLOOD CELL FORMATION (HAEMATOPOIESIS)

Haematopoiesis begins in the embryo and takes place in the yolk for the first 1½ to 2 months of
foetal life. From about 2 months after conception the foetus blood cell production becomes more
specialised and liver and spleen are the main sites, continuing to manufacture blood cells until the
baby is about 2 weeks old. When the foetus is about 6 - 7 months old the most important site of
haematopoiesis is the bone marrow and most bones are involved in blood cell production. From
birth the bone marrow is the major site of blood cell production and infants carry out haematopoiesis
in practically all bones in the body. By adulthood, the only site still active in this regard is the bone
marrow. The main sites of blood cell production are the red bone marrow (myeloid tissue) of the
proximal epiphyses of the humerus and femur; flat bones of the cranium, sternum, ribs, vertebrae,
and pelvis; and the lymphoid tissues. Red blood cells, granular leucocytes (eosinophils, neutrophils,
and basophils), and platelets, are produced in red bone marrow while agranular leucocytes (T-cells,
B-cells, and monocytes) are produced both in the myeloid tissues and also the lymphoid tissues
such as spleen, tonsils, thymus, and lymph nodes. T-cell production, in particular, is stimulated in
times of infection by the thymus.
All blood cells originate from a common nucleated cell called a haemocytoblast or pluripotent stem
cell. This stem cell undergoes differentiation to produce the mixed myeloid progenitor cells and the
lymphoid stem cells. These, in turn, differentiate further to produce proerythroblasts, myeloblasts,
monoblasts, megakaryoblasts; and lymphoblasts. The proerythroblasts differentiate further, losing
their nucleus, and eventually become erythrocytes. Myeloblasts differentiate into myelocytes
22
which, in turn, differentiate into eosinophils, neutrophils, and basophils. Monoblasts become
monocytes, lymphoblasts differentiate into lymphocytes (T-cells and B-cells), and megakaryoblasts
are the predecessors of thrombocytes. During immune system activation, monocytes are
differentiated into wandering macrophages and B-cells enlarge then divide and differentiate into
plasma cells.
Courtesy of “Principles of Anatomy and Physiology” eds Tortora & Anagnostakis
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1. Red Blood Cell Production (Erythropoiesis):
Erythropoiesis is the process by which erythrocytes are formed. Proerythrocytes (also known as
rubriblasts) produce early erythroblasts (prorubricytes) followed by intermediate erythroblasts
(rubricytes) which are the first cells in the sequence to start manufacturing haemoglobin. Next in
the sequence of events is the production of late erythroblasts (metarubricytes), in which
haemoglobin synthesis is at a maximum. The metarubricytes are then converted into reticulocytes
which have lost their nucleus and mature into erythrocytes, usually within 1 - 2 days, once they
have been released into the blood stream from the bone marrow. An enzyme, renal erythropoietic
factor, is released by kidney cells during times when these cells become oxygen deficient. The
erythropoietic factor stimulates the production of the protein hormone erythropoietin by the kidneys
and, to a lesser extent, the liver which, in turn, stimulates the production of erythroblasts in the bone
marrow, thereby increasing red blood cell production. This is a homeostatic mechanism designed
to step up red blood cell production whenever erythrocyte numbers decline, either due to slow
erythropoiesis or increased red blood cell destruction in the body. In either case it is signalled by a
decline in oxygen supply to cells in the body (hypoxia). Hypoxia can be caused by failure to breath-
in enough oxygen (eg. in asthma, high altitudes, inactivity, etc.), smoking, or in conditions of
anaemia. Anaemia has many causes including poor iron assimilation, low iron intake, lack of certain
amino acids, lack of vitamin B12 and/or folic acid, and poor mineral balance (iron, magnesium,
calcium, zinc). In vitamin B12 deficiency, pernicious anaemia occurs. This is primarily due to the
lack of production of intrinsic factor, by the parietal cells of the mucosa of the stomach, which
facilitates absorption of vitamin B12 through the small intestine into the blood stream. Vitamin B12
is also known as extrinsic factor.
Aged and damaged red blood cells are destroyed by phagocytic macrophages present in the spleen
and liver. These macrophages [known as reticuloendothelial (RE) cells] then become the major
source of iron in the body. Transferrin in the plasma transports iron from these RE cells into
erythroblasts in the bone marrow. A small amount of plasma iron also comes via absorption from
the duodenum and jejenum from dietary iron and this is also transported to erythroblasts in the bone
marrow for erythopoiesis. Globin proteins formed by red blood cell destruction are reused by the
body while heme is eliminated. Iron absorption is facilitated through the duodenum and jejenum by
factors such as acid and reducing agents which keep the iron in a soluble form and, particularly, in
its ferrous (Fe++) state rather than the ferric (Fe+++) state. The iron binds to transferrin in the portal
blood for transportation to the bone marrow.
2. White Blood Cell Production:
Leucocytes are produced by differentiation of the primordal haemocytoblast as outlined above. One
feature of leucocytes is the presence of specific surface antigen proteins on their cell membranes.
These antigens, known as Human Leucocyte Associated (HLA) Antigens are unique for every
single individual (except true identical twins) and can be used for identification purposes - say in
forensic laboratories - and compatibility testing of tissues used in organ transplants. HLA antigens
are determined by a single set of genes on a single chromosome in the nucleus (chromosome b).
This set of genes is called the Major Histocompatibility Complex (MHC) and the HLA antigens are
sometimes also known as histocompatibility antigens. Detection and identification of HLA antigens
24
is accomplished by specific antisera tests and, more recently, by the use of a very powerful DNA
technique - Polymerase Chain Reaction (PCR) - in which the MHC complex is amplified and its
sequence determined by electrophoresis of fragments of the DNA produced by hydrolysis of the
amplified material using specific nuclease enzymes. This technique is being used commonly in
forensic cases, paternity suits, and a range of genetically determined diseases in addition to tissue
typing and research laboratories.
During infection or immune system activation (eg. rheumatoid arthritis, lupus erythematosis,
multiple sclerosis, colitis ulcerosa, Crohn's disease, and other autoimmune diseases where the body
turns its immune system against its own healthy tissues) leucocyte production is stimulated. This
leads to an increase in phagocytic activity and production of extra histamines which produce
inflammation in the body. This sets up a vicious cycle as kinins produced by damaged tissues at the
site of inflammatory processes attract phagocytes to the site and these then exacerbate the
inflammation.
Generally, increased leucocyte count will be indicative of infections (bacterial), stress, burns,
autoimmune diseases (above), or inflammation; while decreased leucocyte count will be indicative
of radiation or chemotherapy, certain drugs, or vitamin B12 deficiency. White blood cells develop
under the influence of hematopoietins called Colony Stimulation Factors (CSF’s). There are 4 such
CSF’s viz. macrophage CSF (M-CSF) which stimulates the development of monocytes and
macrophages, granulocyte monocyte CSF (GM-CSF) which stimulates development of
granulocytes and monocytes, granulocyte CSF (G-CSF) which stimulates granulocyte development
only, and multi-CSF, or interleukin-3, which stimulates development of a range of white blood cells,
including the lymphocytes. CSF’s not only stimulate the production of white blood cells but also
enhance their activity so have a boosting action on the immune system. They may aid in the body's
natural defences against cancers, AIDS, and other immune disorders.
3. Platelet Production:
Thrombocytes are produced by the differentiation of megakaryoblasts into megakaryocytes which

fragment into thrombocytes or platelets which are small vesicles consisting of cytoplasmic contents
from the megakaryocytes enclosed by cell membrane from the same cell. They have no nucleus.
Interestingly, Enderlein believed the thrombocytes to be of plant origin, to contain 2 - 8 nuclei and
be a pathogenic form of the endobiont but his ideas in this regard have well and truly been disproven.
Thrombocytes are, in fact, essential for good health and well-being.
VI. BLOOD DISORDERS

1. Anaemia
The most common blood disorder is that of anaemia in which iron levels are either low as a result
of low erythrocyte numbers or low haemoglobin. The clinical definition of anaemia is that
haemoglobin levels are less than 13.5 g/dl in adult males and 11.5 g/dL in adult females and (from
the age of 3 months to puberty) a reading of below 11.0 g/dL in children. Newborn infants generally
have a haemoglobin level of around 15 g/dL so an anaemic indication would be levels of less than
25
15 in the newborn. A reduction in haemoglobin level is often accompanied by a decrease in red cell
numbers and packed cell volume (PCV). The PCV is a measure of the number of red cells present
in the blood and it indicates the volume of red cells which pack down during centrifugation of the
blood under specific conditions. Decreased circulating plasma volume (such as during dehydration)
may mask anaemia while increased plasma volume (eg. during pregnancy) may cause anaemia even
though the red cell and total haemoglobin in the blood is normal. After acute blood loss anaemia is
not immediately apparent as the total blood volume is reduced. With mild forms of anaemia there
may be no symptoms or signs so people can be mildly anaemic without knowing. Thankfully, the
live blood morphology test will enable you to see indications of anaemia prior to it being a
symptomatic problem and thus allowing you to correct a deficiency before it produces clinical
symptoms. For example, macrocytosis (presence of large red cells in the blood) is symptomatic of
early folic acid and vitamin B12 deficiencies; microcytosis (small red cells) indicates poor iron
assimilation; elliptocytes are indicative of low magnesium levels prior to iron deficiency etc.
Variations in erythrocyte size (anisocytosis) and shape (poikilocytosis) are common to anaemia,
even in its mild form. Some of the various sizes and shapes of red cells include microcytes,
elliptocytes (ovalcytes), target cells, macrocytes, burr cells (echinocytes), acanthocytes, fragments
(schistocytes), sickle cells, and spherocytes.
There are a number of different types of anaemia but in all cases the symptoms are much the same.
Fatigue, shortness of breath (particularly on exercise), weakness, lethargy, pallor, lack of
motivation, palpitations, headaches, ringing in the ears (tinnitus), loss of appetite, irritability,
abdominal pain, and cold intolerance are the most common. In anaemia, oxygen carrying capacity
is reduced (less erythrocytes and/or less haemoglobin to carry oxygen around the body) thus
respiration rate is low and consequently less ATP is manufactured by cellular mitochondria leading
to less energy production. Paleness is a direct reflection of the lower haemoglobin levels in the
blood. General signs primarily involve pallor of the mucous membranes (conjunctival mucosa, nail
beds, and skin). Specific signs may be noted for different types of anaemia. For example,
koilonychia (spoon-shaped nails) is common with iron deficiency, jaundice with haemolytic or
megaloblastic anaemia, leg ulcers with haemolytic and sickle cell anaemia, bone deformities with
thalassaemia major and severe congenital haemolytic anaemia. Excess infections or spontaneous
bruising may be associated with neutropenia (low neutrophil counts) or thrombocytopenia (low
platelet count).
Generally, anaemia may be due to either defective blood cell production or excessive erythrocyte
loss. There are three major classifications of anaemia typified by red cell size and shape. These
classifications are: Normacytic, Microcytic, and Macrocytic.
Normacytic anaemia is the result of blood loss, haemolysis, chronic disease, or combined iron and
folate deficiency. The erythrocytes are normal size and colour but are fewer in number than normal.
Microcytic anaemia is due to iron deficiency, Thalassaemia, chronic disease, or sideroblastic

anaemia (a genetic disorder in which haem synthesis is defective due to lack of production of δ-
aminolaevulenic acid synthetase enzyme). Erythrocytes are smaller than normal, often odd shapes,
and frequently are hypochromic (lack colour).
26
Macrocytic anaemia is due to deficiencies in vitamin B12 and/or folic acid, alcohol abuse, liver
disease, cytotoxic drugs, aplastic anaemia (from iatrogenic, industrial, infectious, or genetic causes),
myeloma, and pregnancy. Erythrocytes are larger than normal and may be hypochromic.
a. Nutritional Anaemia
Nutritional anaemia is a direct result of inadequate iron, copper, cobalt, vitamin B12, folic acid and
necessary amino acids. It is frequently related to not only poor intake of these essential nutrients but
also poor digestion/assimilation, hypoglycaemia (in which protein assimilation is reduced), and
other factors which can lead to deficiencies of these nutrients. Nutritional anaemia may be indicated
by the presence of microcytes, macrocytes, and/or elliptocytes; usually in smallish numbers.
Iron absorption from dietary sources is favoured by several factors. These include: ferrous,
inorganic, iron form; acids such as stomach hydrochloric acid (HCl); ascorbic acid (vitamin C);
solubilizing agents such as amino acids and sugars; pregnancy; iron deficiencies; increased
erythropoiesis; and primary haemochromatosis. Factors which reduce iron absorption from the gut
include: ferric, organic iron form; alkalosis and alkaline substances such as antacids and excess
pancreatic secretions; precipitating agents such as phytates and phosphates; excess iron; decreased
erythropoiesis; infection; tea; and desferrioxamine.
The iron intake required to compensate for normal losses from the body varies with age and sex,
and is highest during pregnancy, menstruation, and in adolescence females.
If iron intake is excessive, the transferrin becomes saturated and excess iron is transferred to
parenchymal cells in the liver, endocrine organs, pancreas, and heart. It is most important, therefore,
to re-check the blood at regular intervals if you put someone on an iron supplement.
Iron deficient anaemia is characterised by spoon nails (koilonychia), fissuring and ulceration of the
corner of the mouth (angular cheilosis), and pallor in the mucous membranes (eg. inside of eyelids).
b.Pernicious Anaemia
This anaemia is directly related to vitamin B12 and Folic acid deficiency. Insufficient production
of intrinsic factor in the gastrointestinal tract results in poor absorption of vitamin B12. Gut related
disorders such as surgery-induced deficiency of intrinsic factor, terminal ileal disease, bacterial or
parasitic overgrowth in the gut, pancreatic failure, and administration of drugs which reduce
intrinsic factor will often lead to some degree of pernicious anaemia. Pernicious anaemia is due to
reduced DNA (and thus erythrocyte) synthesis (Megaloblastic anaemia) because of folate
deficiency, cytotoxic drugs, inborn errors, nutritional deficiency in vegans and alcoholics, and
increased requirements during pregnancy. A 'beefsteak' tongue is often associated with this
anaemia.
Pernicious anaemia is often characterised by the presence of very large erythrocytes (macrocytes)
and multi-segmented neutrophils in the blood.
c. Sickle-Cell Anaemia
A genetic defect known as sickle cell anaemia results in a single amino acid substitution in two of
the polypeptide chains in globin (in haemoglobin). In this case valine is substituted for glutamic
27
acid. The result is that, at low oxygen levels, the haemoglobin in these cells tends to crystallise,
drawing the red blood cells into their characteristic sickle shapes. Sickle cell anaemia is most
common to populations that live in malaria infected areas around the world such as Africa, Asia,
and Mediterranean countries. It, interestingly enough, acts to prevent erythrocytes from rupturing
during a malarial attack, thereby conferring a high resistance to malaria on those individuals who
have the trait. Persons with only one gene for this trait (heterozygotes) enjoy the resistance to
malaria without actually suffering from the anaemia while those who inherit both genes
(homozygotes) suffer from anaemia.
d. Haemorrhagic Anaemia
This is a Normocytic type of anaemia due to excessive loss of erythrocytes brought about by blood
loss through some trauma. Menorrhagia (heavy menstrual blood loss), deep wounds, and bleeding
stomach ulcers are some of the main contributing factors to this anaemia. Typically, a low red blood
cell count is noted when the blood is examined.
e. Haemolytic Anaemia
This is due to the premature rupturing of erythrocyte membranes leading to the release of red blood
cell contents into the plasma and the appearance of 'ghosted' cells which consist primarily of an
empty cell membrane envelope. Many genetic and other factors can lead to this condition such as
haemoglobin defects, abnormal red cell enzymes, red cell membrane defects, internal parasites,
toxins, and antibodies from incompatible blood (eg. Rh factor incompatibility in newborn babies).
Other factors include infections, certain drugs (antimalarials [quinines] and sulfonamides such as
salazopyrin), antibacterials (nitrofurans and chloramphenicol), analgesics (aspirin, phenacetin), anti
helminthes (beta naphthol, stilbophen, nitrodiazole), vitamin K analogues, naphthalene, probenecid,
fava beans, and high levels of copper ( eg in Wilson’s syndrome). Mild jaundice, leg ulcers (chronic
cases), and biliary colic (pigment gallstones) are often associated with this type of anaemia. Live
blood analysis will typically reveal many abnormal red cells such as microcytes, fragments, sickle
cells, elliptocytes, hypochromia, poikilocytosis, anisocytosis, and, particularly, pencil cells.
Immune haemolytic anaemia also occurs in the newborn mainly as a result of Rhesus (Rh) factor
incompatibility. Blood from these babies shows nucleated red cells (reticulocytes).
f. Aplastic anaemia
Aplastic anaemia can be due to reduced erythropoiesis (as a result of reduced DNA synthesis) or
destruction of bone marrow cells by chemotherapeutic agents, radiation therapy, toxins, certain
drugs, infections such as viral hepatitis, or tumour cells. Drugs which inhibit enzymes involved in
erythropoiesis (indomethacin used in the treatment of arthritis, and chemotherapy agents such as 5-
fluorouracil, leukeran, cytoxan, alkeran, myleran, purinethol, methotrexate, and velban) are all
known to cause aplastic anaemia. Not only do they reduce red cell numbers but they also reduce the
numbers of white cells and platelets so consequently have a disastrous effect on the immune system.
The medical answer to these iatrogenic (medically-induced) disorders is a bone marrow transplant
which leaves the patient on immunosuppressive drugs for months, or even years after the transplant.
28
During treatment with these immunosuppressive drugs the patient is highly susceptible to
infections.
Microscopically aplastic anaemia produces an array of fragile red cells, elliptocytes, fragments,
reticulocytopenia, granulocytopenia, monocytopenia, thrombocytopenia, and some decrease in
lymphocyte numbers. Oral thrush (candidiasis) is also found in many aplastic anaemia patients.
g. Thalassaemia
This is another genetic disorder in which defective haemoglobin is produced leading to a haemolytic
type of anaemia. Erythrocytes are extremely thin and fragile with large numbers of target cells,
microcytes, stippled cells, and even nucleated red cells.
Thalassaemia occurs primarily in Mediterranean countries.
2. Infectious Mononucleosis (Glandular Fever)
Glandular fever is a highly infectious viral disease caused by the Epstein Barr Virus (EBV). EBV
has also been linked to other disorders such as Burkitt's lymphoma, nasopharangeal carcinoma, and
Hodgkin's disease. Its main occurrence is in children and adolescents but can also affect adults
particularly when under severe stress. It is common to students around exam time! An elevated
white blood cell count and enlarged B-cells which take on the appearance of monocytes are
common indications in the blood. Symptoms include severely swollen glands (particularly in the
neck), extreme fatigue, headaches, dizziness, sore throat, fever, brilliant red throat, stiff neck, cough,
and malaise. Once a person has contracted glandular fever it may re-occur unless they are fastidious
about supporting their immune system and staying healthy. This means a healthy diet, regular
exercise, and colostrum, certain herbs (Echinacea, Astragalus), vitamin (mainly vitamin C), and
mineral (particularly zinc) supplements to boost the immune system.
3. Parasites
A number of parasites can clearly be observed in the blood but many are only seen after staining
procedures using special chemical dyes. Malarial trophozoites can be seen in red cells,
trypanosomes, microfilaria, spirochaetes, and candida yeast and fungal spores are all seen if the
appropriate parasitic infection is present.
a. Malaria
Trophozoites of malarial parasites can be seen in red blood cells and several erythrocytes may be
haemolysed. Thrombocytopenia is also common in acute cases. In chronic cases there may also be
moderate thrombocytopenia and neutropenia due to hypersplenic activity. Consequently, malarial
patients show signs of anaemia in addition to the presence of parasites.
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b. Trypanosomiasis
Trypanosomes are evident in the blood of individuals infected with these parasites. Infection with
Trypanosoma brucei is most common in areas of Africa and South America.
c. Spirochetes
Leptospires are spirochaetes present in the blood during an infection. They are about 7 – 14µ long
and 0.1µ wide and may be seen in live blood. These microorganisms have been linked as causative
agents in a number of diseases including Weil’s disease (a form of haemorhhagic jaundice), canicola
fever, “seven-day fever”, Akiyami, “swamp fever”, “cane fever”, and others.
4. Thrombocytopenia
Low platelet count may be due to low erythropoiesis, congenital disorders, overactive spleen
(hypersplenism), viral infections, drug reactions, megaloblastic (aplastic) anaemia, massive
haemorrhage, haemolytic uraemic syndrome, or immune mediated thrombocytopenia. Easy
bruising and poor blood clotting are the most common symptoms. Henoch-Scholein purpura is one
of the many forms of thrombocytopenia.
LBA reveals practically no platelets.
5. Thrombocytosis
High platelet count is usually asymptomatic but bleeding tendencies are sometimes noted. In severe
cases gangrene can occur in the extremities. Splenectomy, reaction to surgery, response to blood
loss, severe infections, and certain tumours may lead to thrombocytosis.
Excessive numbers of platelets, often aggregated into large masses are often seen in the blood of
these patients. In the Bernard Soulier syndrome very large platelets are also present.
6. Haemophilia
Lack of clotting or poor clotting of blood can lead to haemorrhage. Haemophilia is a genetic disorder
carried by females. Von Willebrand's disease is more common than haemophilia and is due to a
platelet vessel wall defect which slows the clotting time.
7. Scepticaemia
Scepicaemia (bacteraemia) is a bacterial infection in the blood usually as a result of a severely

compromised immune system in patients with long-standing chronic, degenerative, diseases such
as cancer, AIDS, and certain forms of leukaemia. It is frequently a terminal condition.
30
8. Fungaemia
Fungaemia is a fungal infection of the blood, again, usually as a result of a severely compromised
immune system as with scepticaemia.
8. Other
Microfilaria of both Bancroftian filariasis and B. loiasis may be observed in peripheral blood.
VII. THE HISTORY OF THE THEORY OF DISEASE
Some of the early pioneers of biological science included Pasteur, Béchamp, Bernard, Koch, and
the philosopher René Decartes. These individuals made an immense contribution to the
development of biological science at a time when practically nothing was known about the structure
of the cell and its contents. Despite the limited knowledge they shared they came up with some very
interesting findings that led to hypotheses that could still be adhered to today if it were not for the
discovery of DNA, RNA and their subsequent composition and structure.
Geronimo Fracastorio (1483-1553), an Italian physician and poet) first published a work in 1546
which alluded to the true nature of disease. He divided diseases up into:
a. those which infect by immediate contact
b. those that infect through intermediate agents
c. those that infect at a distance through the air
He supposed that infecting organisms were of a viscous or glutinous matter similar to colloidal
states of substances described by modern physical chemists. The organisms were too small to be
seen, were capable of reproduction in appropriate media, and became pathogenic through the action
of animal heat.
In 1683, Antonius van Leenwenhoek, a Dutch naturalist, observed in a microscope of his own
manufacture small moving bodies in water, saliva, dental tartar, and other liquid media which he
called animalcula (or animicules). These rod shaped and spiral shaped organisms were the first
described microorganisms.
In 1762, M. A. Plenicz, a Viennese physician published a germ theory of infectious disease. He

maintained that there was a specific infecting organism for each disease, that microorganisms were
capable of reproduction outside of the body, and that they might be conveyed from one place to
another via the air. This became the theory of Monomorphism (only one shape and size for each
microorganism).
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Claude Bernard (1813 – 1878)
One of the most fundamental and significant findings in biology in the 1800’s was made by Claude
Bernard, a zoologist, who discovered that animals have the inate ability to maintain constant
composition of the extracellular fluid – the milieu intérieur. It is this ability that is one of the most
significant advances in evolution, allowing animals to become virtually independent of their
external environment.
Louis Pasteur (1822 - 1895)
Pasteur was perhaps one of the foremost pioneers of microbiology along with Robert Koch and
Ferdinand Cohn. He was credtited with the following successes:
a. The finding that tartaric acid crystals came in two asymmetric forms that were mirror images
of each other thus establishing the chirality of molecules.
b. Confirmation of the Germ Theory of disease*.
c. Creation of the first vaccine for rabies.
d. Sterilization of milk by the process later named Pasteurization.
e. Reduction in the mortality rate of children from puerperal fever.
f. The process of fermentation was due to the growth of microorganisms – not spontaneous
generation**.
g. Applied the processes of vaccination and immunology.
Despite the fact that cell structure was unknown, Pasteur was able to foresee that cells were
composed of a range of organic compounds that we now know as proteins, enzymes, phospholipids,
polysaccharides, fats, fatty acids, and nucleic acids. He ‘proved’ the germ theory of disease and
promoted monomorphism. *In fact, he claimed them as his own despite the fact that Plenicz had
published the essence of these theories almost 100 years earlier. Among his many discoveries was
that transmission of disease by salmonella (and other bacteria) could come via the consumption of
cow’s milk (which is most probably why many of his contemporaries recommended that we do not
32
consume cow’s milk – a recommendation that remains to this day by some health practitioners). To
avoid the problem of infection being transmitted through cow’s milk, Pasteur discovered that
heating the milk to near boiling for a specified time was able to destroy the microorganisms in the
milk and render it safe for consumption (Pasteurization). Pasteur did not discover the process of
vaccination, this was done some years earlier by Edward Jenner and his first anthrax vaccine was
made using the method of one of his rivals – Jean Joseph Henri Toussaint (even though Pasteur
claimed it as his own). **The process of fermentation was established as involving microorganisms
by Béchamp when Pasteur clearly still believed in spontaneous generation but later Pasteur also
claimed this discovery as his own.
Antoine Béchamp (1816-1908)
Microorganisms in living blood were discovered originally by Antoine Béchamp in the mid 1800’s.
Béchamp carried out his research at around the same time as Louis Pasteur and actually published
findings related to fermentation and infection by ‘microbes’ prior to Pasteur. It has been claimed
that Pasteur actually plagiarized much of the work of Béchamp (40). Be that as it may, Béchamp’s
main discovery was that he described microzymas as the smallest living unit (much smaller than
bacteria) and that, in response to changes to the internal environment of the body (the milieu), these
microzymas could transform themselves into bacteria which could either destroy
decaying/damaged cells and tissues in the body as a form of protection or become pathogenic and
lead to disease. So, Béchamp’s major contribution to cellular biology was that disease could come
from within the individual as well as from external pathogens. When an animal or plant dies
Béchamp argued, the microzymas assist in the process of decay and breakdown of the now non-
living biological material. An experiment with a dead kitten showed the microzymas to be present
around the region where the carcass had been completely degraded long after the carcasses had been
decayed.Microzymas are not destroyed because they were found to be present in ancient geological
calcereous (limestone) rocks that were many thousands of years old. Microzymas supported the
process of fermentation and are the original progenitors of all cells. Béchamp originated the theory
of pleomorphism (several different shapes for each microorganism) and argued that the number of
microzyma species was enormous and each one had its own pleomorphic cycle.
Amongst the many discoveries attributed to Béchamp were the following:
1. All living things contain microzymas which are the basis of all living things.
2. Mycrozymas produce proteins he called zymas (enzymes) that support all processes of
fermentation, digestion, and assimilation.
3. Mycrozymas are the “third element of the blood”, along with red blood cells and white
blood cells, and are involved in the production of fibrin and the coagulation process.
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4. Fibrin is a mixture of albuminoid proteins, fats, and microzymas. It is formed from a soluble
protein present in the blood plasma which he called fibrinin (fibrinogen?).
5. Fibrin contains microzymas as a central (“nuclear”) component which is not seen under
light microscopy due their small size (<0.5µ diameter). It is only after the process of
coagulation proceeds that the microzymas may be observed.
6. Ferments require nutrients, particularly of a proteinaeceous nature, in addition to sugar and
water to support fermentation. However, in the absence of proteins fermentation of sugar is
supported by nitrogen from air.
7. Organic matter is essentially mineral matter containing carbon as one constituent.
8. Organic matter is profoundly distinct from organised matter. The chemist can manufacture
organic matter but is powerless to organise it. Organisation of matter resides, primordially,
in pre-existing living organisms.
9. Schwann’s ascertain that germs exist in the air (environment).
10. Air-borne bacteria are responsible for ‘ruining’ alcoholic fermentation of grape musts by
yeasts.
It is argued by Douglas-Hume (40) that Béchamp’s microzymas may, in fact, be chromatin as he

describes it as the basis of all life and containing the chemical information capable of determining
the characteristics of the organism it is derived from. Microzymas are species and even organ
specific according to Béchamp so they do somewhat fit the chromatin mold.
Günther Enderlein (1872-1968)
Enderlein was a contemporary of Béchamp and extended his work on pleomorphism even though
the scientific community had already fully accepted Pasteur’s germ theory of disease. Enderlein
described the microorganisms he saw by dark field microscopy in the blood as endobiont which
was able to take on many different shapes and forms that he named protits, symprotits, chondrits,
filum, thecits, etc. and assigned the presence of higher forms of these microorganisms in the blood
to various disease states. He ascribed their development to a direct result of pH variations in the
milieu, exposure to, or ingestion of, preservatives, artificial chemicals, agricultural chemicals,
environmental pollutants, and, above all, dietary factors.
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Wilhelm Reich (1897-1957)
Reich studied the works of Sigmund Freud and, while investigating the bioenergetic influences of
human emotion on sexuality discovered a particle in blood which he named the bion. His bions
were able to withstand autoclaving at temperatures exceeding 1,500ºC and he believed that it was
at the border between living and non-living matter – just like Béchamp’s microzymas and
Enderlein’s protits. Reich theorized that there must be two different kinds of single-celled
organisms viz:
a. Those that were life destroying and formed through decay, and
b. Those that were life promoting and formed from inorganic material that comes to life
He found that bions from healthy individuals emitted a blue colour (that of orgone) and showed
energetic movement while those from diseased individuals were smaller, lancet-shaped dark forms
which he named T-bacilli. These T-bacilli were found in cancer patients. Reich concluded that the
orgone energy diminishes with aging and/or injury causing cells to undergo “bionous degeneration”,
leading to eventual death.
Gaston Naessens (1924-2005)
Naessens, who invented a microscope that is capable of observing live blood cells and elements at
magnifications of up to 20,000 to 30,000X magnification (the Somatoscope) gave most probably
the same microorganisms different names (somatides, spores, bacterial forms, globular forms, yeast
forms, ascospore forms, mycelial forms, etc) and proposed a life cycle (the Somatide Cycle)
involving these elements as they continue to grow within the blood in response to changes in the
milieu. Béchamp stated that microzymas are the smallest of all life forms and essential to all life,
Enderlein called his smallest living unit the protit/colloid, Reich named his smallest ‘living’ unit
the bion, and Naessens claimed that life itself is not possible without the somatides.
Despite their different nomenclature Béchamp, Enderlein, Reich, and Naessens all propose:
a. The smallest living unit is not the cell but rather a much smaller body that is essential to all
life (protits, somatids, bions).
b. Under certain conditions this smallest unit of life is capable of undergoing pleomorphism
into larger microorganisms that can be either beneficial, or detrimental, to the health of the
individual.
Phillipa Uwins
In the early 1990’s evidence suggested that very small microorganisms (much smaller than the cell)
may have been present in meteorite rocks from Mars that were found in the Antarctic. More recent
research by Dr. Phillipa Uwins at the University of Queensland (150) has identified very small (20
– 100 nanometres diameter), living, microorganisms similar to those described in the early 1990’s
to be present in ancient rocks of a calcereous nature found in the North West region of Western
Australia . These micro-organisms, called nanobes, can only be seen under the electron microscope
at around 25,000X – 100,000X magnification and are composed of both membranous and DNA
35
material. Under the right conditions they grow and enlarge to resemble fungal forms. Maybe these
are the microzymas described by Béchamp over 150 years ago? Under the light microscope
(magnification up to around 2,500X) microzymas are invisible but we can see the larger
microorganisms that they develop into as a result of changes in the milieu.
VIII. PLEOMORPHISM
1.History:
Antoine Béchamp studied ferments and argued that the smallest living unit is not the cell but rather
a microorganism that he named the microzyma.
Microzymas are described as:
a. Non-perishable and indestructible

b. The cause of fermentation
c. The living unit from which all other micro-organisms arise
d. Present in all living things – human, animal, and plant
e. The transition between non-living and living matter
From the research of Béchamp came an alternate view of disease to that promoted by Pasteur.
Rather than the simplistic view of the Germ Theory of disease (monomorphism - in which all
disease comes via infection by external microorganisms; each one of which is a separate and unique
species and causes a specific disease) Béchamp initiated the idea of the Cellular Theory of disease
in which microzymas, under specific pathogenic influences can develop into bacteria which have
putrefactive and fermentive properties. According to Béchamp, microzymas, are essential to all life
and can live in harmony with their host until there are changes in the milieu which lead to these
‘symbiotic’ microorganisms changing into larger, pathological, microorganisms that, in turn, bring
about disease. In this case disease initiates from within the host rather than from exposure to an
external pathogen. This is the theory of pleomorphism (one microorganism changing into another).
Of course, once the medical establishment accepted the ideas of Pasteur rather than those of
Béchamp, pleomorphism was ‘swept under the carpet’ despite the fact that it has been revealed that
Pasteur reportedly plagiarized much of the work of Béchamp and made it his own - even though he
came to different conclusions about the theory of disease. All Haematology texts list
microorganisms that undergo pleomorphism in Nature and Dr. Lida Mattman extensively covers
the cell wall deficient forms which all undergo pleomorphism in her excellent book on stealth
pathogens (100).
The blood, according to Béchamp, is not a sterile environment but rather a milieu containing
microorganisms which live in harmony with their environment as long as the host remains in a good
state of health and the blood milieu is at the ideal pH of around 7.4. If the blood pH changes to
‘acidic’ (< 7.3) or strongly alkaline (> 7.5), or other changes take place in the milieu that are
potentially pathogenic (exposure to, or digestion of, artificial chemicals, preservatives, drugs,
pollutants, or poor diet) then these ‘friendly’, apathogenic microorganisms undergo developmental
changes to become pathogenic microorganisms that bring about disease states in the host. Enderlein
36
extended this work and added the hypothesis that both the milieu and the microbe were important
to the state of health of an individual.
Claude Bernard a noted physiologist at that time was fully aware of the conflict between Pasteur
and Béchamp and was quoted as saying “No gentlemen, the microbe is nothing; the milieu is
everything”. On his death bed it is also reported that Pasteur said “Bernard was correct. The microbe
is nothing; the milieu is everything” thus indicating that he agreed with the research of Béchamp
and that, at least some, of his ideas were vindicated! However, it is now obvious that it is not only
the milieu and the microbe that are important but also body (immune function), mind (emotional
state), and spirit (belief system).
What is the milieu (or terrain)? The milieu is everything that surrounds, or fills, an organ or tissue,
in the body. It is the medium in which cells and tissues are bathed and is made up of water, solutes,
sugars, gases, amino acids, fatty acids, and any other compound required for the nutrition of that
organ or tissue. The milieu refers to all extra-cellular fluid which includes the interstitial fluid and
the blood plasma. Extra-cellular fluid makes up about 20% of total body weight, 75% of which is
interstitial fluid and the other 25% blood plasma. All microorganisms have specific requirements
for the milieu to allow them to grow so unless the milieu fulfils those requirements there will be no
growth of those microorganisms. Once the milieu changes due to alterations in eating patterns,
exposure to artificial chemicals, radiation, etc, and becomes an ideal medium for any specific
microorganism then that microorganism will multiply rapidly. For example, most pathogenic
bacteria grow best at around the ideal pH of blood (approx. 7.4) whereas streptococci require an
acid medium of pH 5.43 to grow - even a pH of 5.46 will not support their growth. However, other
microorganisms (eg fungi) will, and do, grow at pH 5.46. In the case of pleomorphism, even more
subtle changes in pH of the milieu are believed to lead to microorganisms developing from one
form to another.
Interestingly enough, we now know that many bacteria and fungi have forms that can live under
very harsh conditions until the medium is conducive to their growth and development. What
Béchamp was probably observing was the growth of these microorganisms from innocuous forms
to pathogenic bacterial and/or fungal forms once the condition of the milieu changed to a state
favourable to their growth and development.
Günther Enderlein was a long term contemporary of Béchamp and, after Béchamp’s death,
extended his research work on the blood using darkfield microscopy. His work is detailed by Maria
Bleker in her book “Unappreciated Friend or Unsuspected Foe” (14). In 1916, while studying
typhus, Enderlein noted the tiniest moving particles in the blood which entered into union with
higher organized bacteria and instantly became invisible. He surmised that sexual union had taken
place between these minute particles and the bacteria that led to the formation of not higher forms
but rather lower forms that became invisible to the naked eye under dark field light microscopy.
The vigorously moving particles had a flagella and he named them spermits. He argued that it was
through this means that the body was able to rid itself of potential pathogens (the results of which
were eliminated through the normal excretory mechanisms). Enderlein also proposed that all
microorganisms possess a developmental cycle that starts with the primitive phases (apathogenic),
37
changes into the bacterial phases (prepathogenic and pathogenic), and finally culminates in the
fungal phases (highly pathogenic).
Primitive phases require a strongly alkaline milieu, bacterial phases require a mildly alkaline milieu,
and fungal phases require an acid milieu. At the lowest point of this cycle there are apathogenic
microorganisms he called protits (immovable proteins of plant origin) and at the highest point of
the cycle there exists highly pathogenic fungus. Between the lowest and highest points of the cycle
there exist innumerable growth forms amongst which are the bacterial forms. Enderlein was first to
offer proof that bacteria are nucleated and that they multiply by both sexual and asexual means
however he was never credited with these discoveries probably because he never published any of
his findings in peer reviewed scientific publications – only personal notes and articles. His findings
were either totally discarded by the medical and microbiological scientific community - or unknown
to them.
According to Enderlein there are two ever present microparasites that are constant companions
(symbionts) of all mammals including the human species:
The primary symbiont (or endobiont) culminates into the fungus Mucor racemosus Fresen
via its highest bacterial form Leptotrichia buccalis.
The secondary symbiont, tubercle bacillus or Koch’s bacillus culminates into the fungus
Aspergillus niger (van Tieghem) via its higher bacterial form Micobacterium tuberculosis
syn. Scerothrix tuberculosis.
In healthy blood only the primitive phases of these microorganisms exist, establishing themselves
in the blood plasma, the blood cells, as well as in all corporal humours and tissues. Some of the
primitive phases of Mucor racemosus are of a fibrin nature while others are spermit in nature and
they are of great importance in bodily defence mechanisms and blood viscosity. In the form of
thrombocytes they also play a vital role in blood coagulation mechanisms.In its advanced forms,
the endobiont frequently expresses itself as a possible cause of cancer but may also manifest itself
in many other diseases, mostly associated with circulation, blood clotting, and the heart. According
to Enderlein, endobiont expressly devours proteins of an animal source so he recommends a low
animal protein diet.
The primitive phases of Aspergillus niger are of importance in the regulation of calcium metabolism
and within the citric acid (Kreb’s) cycle and development into the higher forms within the
Aspergillus niger cyclode leads to diseases of the skeletal system, lymph system, connective tissues,
mucous membranes, or to cancers.
The two symbionts described by Enderlein are believed to be transmitted diaplacentally to

mammalian embryos and stand in a determined relationship to each other and complement and
replace one another mutually.
38
According to Enderlein, the most primitive form of each microbial form (symbiont) is the protit, an
immovable protein colloid which has a diameter of approximately 0.01µ. Depending upon the state
of the milieu the protits are able to develop into various forms:
a. The filum or fila is a tiny, one dimensional, thread-like body formed from the linear union
of a number of protits and are not individually visible in the darkfield light microscope due
to their miniscule diameter of only 0.01µ.
b. The symprotit which is a two- or three- dimensional primitive granule formed from the
spherical union of a number of protits and has a diameter of around 1µ.
c. The chondrit, a dumb-bell shaped formation consisting of two symprotits and a single filum.
The chondrit stage is characterized by the permanent change between filum and symprotit
and is the collective term for the very first primitive phases (chondritosis). Microchondrits
are apathogenic whereas macrochondits are pathogenic. The latter are most probably rod
form bacteria or L-forms. One macrochondrit is the cell wall deficient form of the tubucle
bacillus Mycobacterium tuberculosis which is part of the Aspergillus cycle.
39
d. Fibrin according to Enderlein is the end product of development of the filum via filit and
filit dendroids to fibrin.
40
Protit (invisible)
Fila (invisible) from linear connection of protits
Filum:
Filum Dendroid:
Fibrin:
Lipid Ribbon:
e. The gonit (gonidia) – these are formed by a process of budding off from synascits (very
long rod forms of bacteria). They can be 0.6 - 1µ in diameter and consist of a spherical ball
shape with a single nucleus – similar to the mychit.
41
f. The Oit – this appears as a spherical form with a ‘wart-like’ protrusion sticking out from its
surface. The oit is the unfertilized bacterial egg and is, according to Dr. Thomas Rau, at the
very first branch point where the Mucor cycle branches off into the Aspergillus cycle. Oits
are approximately 0.6 - 1µ in diameter and are produced from the Gonit during meosis.
g. The spermit, the sex cell consisting of a round head about 0.25 – 0.35µ in diameter and a
whip-like tail (flagella) which can be up to 3µ in length. These forms act as bacteriophages
that destroy bacteria that exist in the Mucor cycle. Enderlein argued that they unite sexually
with the primary nuclei (mych) of bacteria rendering the bacterium non-pathogenic and
degrading it into apathogenic primitive phases (spermits) of the cyclode. These nearly
invisible bodies are specific to the Mucor bacterial forms – see later (p 86). Spermits and
oits can also undergo sexual union to produce gonits.
h. The mych is a symprotit which has chromatin material (trophoconie and trophosomes)
attached to it, the combined unit functioning as a bacterial cell nucleus.
i. The mychit – the first bacterial cell having only one nucleus. Note that these microorganisms
are cell wall deficient.
j. The cystit – a larger mychit with a polydynamic nucleus. These forms are also cell wall
deficient. The cystit can develop by division of its nucleus to form thecits, colloid thecits,
and dioecothecits:
42
Cystit:
Thecit:
Colloid Thecit:
Dioecothecit:
Alternatively, the cystit can divide as a whole cell to produce basits (coccal form bacteria)
and ascites (rod form bacteria).
43
k. The basit – a coccal bacterial form with 1 – 2 nuclei.
l. The ascits - bacterial rod forms with 2 – 8 nuclei lined up in a row within the bacterial
cytoplasm.
m. The Synascit which is a collective term for all bacterial developmental stages in which the
nuclei are disordered. These structures are possibly early fungi hyphal forms but may also
be developmental stages of mycoplasmas and/or L-forms.
44
n. The thecit which is a mychit with more than 8 nuclei formed by division of the nucleus of
the cystit. Thesits, colloid thesits, dioecothecits, and thrombocytes, according to Enderlein
are all formed by division of the nucleus (mych) of a cystit.
o. The thrombocyte – a mychit with 2 – 8 nuclei. He also described thrombocyte symplasts

which are, in fact thrombocyte, or platelet, aggregations.
45
p. The colloid thecit which is a cell filled with invisible colloids and moving filum around the
surface of its entire diameter.
q. The dioecothecit which is a colloid thecit filled with miniscule ‘proto-nuclei’ which are
possibly spermits and microchondrits and they, therefore, act as a reserve of bacteria
fighting agents.
46
r. The symplast - the merging of all possible phases (even inside of blood cells) for the purpose
of copulation. Symplasts are aggregations of blood elements. Erythrocyte symplasts are
aggregated red blood cells, thrombocyte symplasts are aggregated platelets, Leucocyte
symplasts are white blood cell aggregates, and filit symplasts are fibrin aggregates. A
thrombocyte sympast is shown below:
47
s. Sclerosymprotitsymplasts are most likely pseudocrystals.
t. The systatogenie – the drive of primitive biological units to merge directly to form a more
stable higher form.
Many of the microorganisms that Enderlein described in the blood were most probably cell wall
deficient forms of different stages of development of Mucor racemosus and they bear a great
similarity to L-Forms of bacteria, Mycoplasmas, and cell wall-deficient (CWD) forms of Candida
albicans plus other fungi including Aspergillus and Penicillium. There are, however, some forms
seen in the blood (dendroids, drepanids, colloid thecits, dioecothecits, etc) that are uniquely different
from any documented forms of microorganism so they are still noted as Enderlein structures.
L-Forms are bacteria that have lost their cell wall due to various means such as treatment with
antibiotics, lithium, and other substances that damage the bacterial cell wall. They are as small as
0.1µ in diameter at their smallest and up to as long as 70µ when present as long thread, or filament,
forms. They exhibit extreme pleomorphism.
Mycoplasmas are naturally occurring cell wall-deficient microorganisms that are mostly seen in the
blood as round objects of around 0.05-0.3µ diameter but can readily assume many different forms
(pleomorphism). These microorganisms can appear as coccal forms, rod forms, hyphal forms, and
thread forms of up to 100µ in length. They differ from L-Forms because they are naturally
occurring cell wall-deficient bacterial forms and which have an absolute requirement for
cholesterol and other sterols for their development and reproduction. Some forms of mycoplasma
also have a polysaccharide tail that helps them attach to tissues that they infect.
These factors, combined with the fact that certain ‘fungal’ forms may be seen in the blood, would
have reinforced Enderlein’s conviction that each microorganism had many forms during it’s growth
cycle and was able to change from one form to another during either upward or downward
development of that microorganism. Be that as it may, whatever we call the forms seen in the blood,
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Enderlein made a significant contribution to microbiology and Sanum formulas that developed from
his theory have proven to be very effective in the treatment of disease states.
According to proponents of Enderlein’s theory, there are three fundamental errors that still hold
sway in modern day medicine regarding the nature of things and biological relationships that are
the cause of disease in general and chronic disease in particular. These are:
a. The theory of monomorphism first put forward by Ferdinand Cohn in 1870 (and adopted
by Pasteur) that there is only a single growth and reproductive form for each microorganism.
b. The idea first put forward by William Harvey in 1651 that the cell is the smallest functional
biological unit.
c. The idea put forward by Virchow and adopted by Pasteur in 1873 that the blood is sterile.
According to Enderlein all chronic disease is based on the development of the endobiont into higher
(bacterial and fungal) forms. He claims that there is only one disease – constant over acidification
of the blood – which disturbs the central regulation of the human body, disorienting it, and which
is largely due to living, and eating, badly. Foods high in animal protein (meats, fish, eggs) cause the
over acidity. According to Enderlein, a Lacto-vegetarian diet is the correct diet nutritionally and
physiologically because it lowers acidification. Healing of disease is only possible when the body
regains its lost regulators ie. the primitive apathogenic developmental forms (spermits and
microchondrits) which are able to metabolise the higher parasitary developmental forms through
copulation and subsequently eliminate them from the body through the elimination organs (kidney,
lungs, intestines, skin). Again, perhaps the microchondrits observed by Enderlein were, in fact, L-
Forms of various bacteria or mycoplasmas present in the blood present in their apathogenic forms.
Gerner (60) isolated what Enderlein described as symprotits from live blood and identified them
using 2-Dimensional gel-chromatography and biochemical analysis. He found that the symprotits
were, in fact, not a living microorganism but rather a protein structure in which globin was the main
component. The identified protein composition most closely resembled that of Heinz bodies
(denatured haemoglobin) and is thought to be formed by the aggregation of hemichrom of old, or
damaged, erythrocytes in the blood of individuals who have health problems/disease. Interestingly,
Enderlein also described these bodies as “protein lumps” that “devoured’ animal protein. Could it
be that what he observed was an aggregation of globin proteins/ hemichrom to produce larger and
larger forms that he deemed to be ‘development’ of the endobiont (symprotits, macrosymprotits
etc) into higher forms? Enderlein stated: “The smallest living unit in the body is not the cell but the
colloid.” The name ‘colloid’ is also interesting because Fracastorio, some 350 years earlier (in
1546) described infectious organisms that cause disease as being “of a nature of viscous or glutinous
matter, similar to colloidal states” of organic substances. It is also interesting to note that colloidal
substances were shown by Robert Brown in 1827 to exhibit sporadic movement when suspended
in fluids and viewed under the microscope. This movement came to be known as Brownian
movement. Both Béchamp and Enderlein were very aware of Brownian movement so they were
extremely careful to make sure that the ‘microbes’ they observed in the blood were not inanimate
colloidal substances (protein in nature) but were, in fact, living microorganisms.
49
Like Béchamp’s microzymas and Naessen’s somatids, Enderlein’s colloids (protits) cannot be
killed at temperatures up to 350C or down to -70C. They are relatively indestructible. Is it possible
that these structures are spores of bacteria, yeast, or fungi?
From the work of Béchamp, Enderlein, and Naessens a number of microorganisms were observed
in the blood that appeared to not fall into the ‘normal’ categories of identifiable bacteria, yeasts, or
fungi. These microorganisms have been largely ignored by the medical and scientific community
for many decades but are worth mentioning here because most of you will be exposed to the dark
field light microscopy of the blood as documented by these individuals and should be able to draw
your own conclusions as to their importance and validity.
As a result of his work on the blood Enderlein developed a treatment protocol involving the use of
isopathic remedies which became known as Sanum Therapy and which offers the practitioner a
useful way of treating a number of maladies in response to the observation of certain
microorganisms in the blood under dark field microscopic examination. It is possible to use Sanum
Therapy without a dark field microscope but extensive use of symptomatology and diagnosis and
the process of systematology are required by the practitioner. Sanum therapy is outlined later in
these notes on Dark Field Live Blood Microscopy.
In the 1930’s Royal Raymond Rife developed a microscope which he named the Universal
microscope and he claimed that it could allow the observation of living cells at up to 60,000X
magnification – greater than that achievable by the electron microscopes of the day! With this
microscope he was able to observe live viruses and their reaction to certain stimuli. He also recorded
the observation of viruses changing form and bacteria changing into viruses which was taboo to the
orthodox medical fraternity who blindly followed the germ theory of Pasteur. Rife also developed
a machine capable of ‘zapping’ microorganisms with specific radio frequencies capable of vibrating
the microorganism violently at its own unique frequency until it burst and was killed. Using this
technique he was able to successfully treat a number of diseases including cancer but because he
worked in direct conflict with orthodox medicine and the drug companies, he earned their wrath
and was subsequently discredited and basically shut down. He died an alcoholic at the age of 92.
Fortunately his work attracted the interest of several forward thinking doctors in his hay day and
they secreted his inventions and technology away so that it could be used by ‘alternative
practitioners’ at a later date. It is still available today but not sanctioned by the FDA in the USA or
the TGA in Australia.
In the 1940’s Gaston Naessens also developed a powerful microscope, which he named the
Somatoscope, capable of up to 20,000 – 30,000X magnification of living bodies. His work
complemented that of Béchamp and Enderlein and he developed the Somatide Cycle from extensive
observation of the blood and blood cell elements. His Somatide Cycle is very similar to Enderlein’s
Cyclogeny of Bacteria although they have different names for the various microbes and miniscule
bodies that they observed in the blood. In common with Enderlein and Béchamp is the fact that
Naessens believes the biological system is weakened by exposure to chemical pollution, ionizing
radiation, electromagnetic fields, poor nutrition, accidents, shock, depression, and many more
factors which, in turn, leads to development of the process of pleomorphism to produce bacterial
forms, yeast forms, and fungal forms, that cause disease.
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2.Pleomorphism vs Monomorphism
Both the Germ Theory of Pasteur and the Cellular Theory of Béchamp have some short-comings in
the light of modern day research developments.
a.The Germ Theory:
i. assumes that the milieu, or terrain, of the body is unimportant

ii. assumes that all disease is as a result of infection by pathogenic microorganisms from the
external environment only
iii. is based on specific microorganisms causing each specific disease
iv. ignores the importance of the nutritional status of the individual
v. is the basis of vaccination which is known to have its problems regarding safety and efficacy
vi. is based on monomorphism and yet we know that some microorganisms can assume a
number of different forms ie. are pleomorphic.
b.The Cellular Theory:
i. ignores the fact that many diseases are caused by infection by external microorganisms
ii. does not account for the presence of CWD forms (L-Forms, mycoplasmas, yeasts) in the
blood
iii. discounts the importance of the immune system in fighting disease
The theory of extreme pleomorphism (one microbial species changing into another) was
discarded by Enderlein but pleomorphism is a fact of life despite the monomorphist’s
arguments. There are reports in the modern literature that keep the debate alive. For example,
Theobald Smith, an eminent bacteriologist, isolated a bacterium from pneumonic lungs of
calves that stimulated actinomycoses and which apparently exists in three different forms: a
bacillus, a coccus with either an endospore or an arthrospore phase, and a combination or
conglomeration of all three (142). More recently, Wood and Kelly (162) showed that a
Thiobacillus sp.of bacterium varied markedly in morphology in response to environmental
conditions and Reding and Leop (125) found that Bradyrhizobium underwent pleomorphic
changes induced by dicarboxylate. Pease (118) and Pease and Pease and Tallack (119) also
reported on a complex life cycle in bacteria that were associated with malignancy and appeared
to be a permanent endoparasite of man, often present as L-Form symplasts.
What is important to remember is:
i. disease can come as a result of infection by external pathogens or from within the individual
ii. the state of the milieu is most important
iii. microorganisms will only grow if the medium (the milieu) is in an ideal condition to support
their growth
iv. disease is more a condition related to poor nutrition than it is to infection
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v. the immune system is most important in determining whether or not we become ill – it is
our defence against disease caused both by external infection and internal growth and
development of microorganisms
vi. the blood is not a sterile medium – even healthy individuals can have microorganisms
present in their blood
IX. CONTROVERSIES IN LIVE BLOOD ANALYSIS

There are two main controversies that exist in the world of Live Blood Microscopy that divide
practitioners and set up various ‘camps’ who claim that they, and only they, have the real
answers and that all other ‘camps’ are wrong in their interpretation of changes in blood element
morphologies. Thus we have the ‘camps’ made up of devotees of Bradford’s High Resolution
Blood Morphology (HRBM®), Hoekstra’s Hemaview, Young’s New Biology Live Blood, and
Enderlein’s Dark Field Live Blood, and Coyle’s Nulife Sciences Live Blood. All of these
techniques have something to offer the practitioner and the patient but none of them are the
complete answer. Let me explain.
The two main controversies in Live Blood Microscopy are:
1. Where do microorganisms present in blood originate from? and

2. Do candida spp exist in the blood of ‘healthy’ individuals?
1. Where do microorganisms present in the blood originate?
Pasteur claimed that the blood was a sterile environment and his concept of monmorphism
suggested that all microorganisms originate from the environment, entering the blood through
various means such as the airways, gut, skin, or mouth. This concept has been well proven over
many years of scientific research as, at least, one source of infection and is the concept adopted
by mainstream medicine. The main problem with this theory of disease is that it does not take
into account the state of health of the individual (immune competence, homeostasis, emotional
stability, belief in self, the HPA axis, or spiritual strength) consequently it does not explain
how, even though we all are constantly bombarded with microorganisms of all types, some
people succumb to their pathogenicity while others do not. After several years of scientific
research mainstream medicine was able to arrive at the conclusion that our immune system was
our major protector from infection but, to this day, they still ignore the other real factors
involved in protection from disease caused by external microorganisms. The most significant
factor that has led to better health is good hygiene. Recent research is now pointing to the
importance of the gut flora in relation to a number of diseases and supporting the gut flora has
been shown to be effective in combating such diseases as multiple sclerosis, allergies, type I
diabetes, rheumatoid arthritis (63), colon cancer and inflammatory bowel disease (65), and
Crohn’s disease (61).
The Enderlein theory claims that there exist two symbiotic forms of microorganism in all
humans – Mucor racemosis Fresen and Aspergillus niger. These two symbionts were argued
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to be constantly present in all cells of the body (even germ cells) and are transmitted trans-
placentally. The many elements that Enderlein observed under dark field microscopy were,
according to him, all various forms of these symbionts, some of which were apathogenic and
others pathogenic. His major contribution to the theory of disease was to introduce the concept
of how both the microorganism and its environment (the milieu) were important in
explaining the process of disease and that both needed full consideration in order to explain
how the body was able to achieve and maintain good health. Prior to Enderlein, Béchamp had
argued it was the milieu and Pasteur argued it was the microbe! Enderlein was a biologist who
was not medically trained but carried out almost 60 years of painstaking research and
observation of elements in the blood and made drawings of his findings. Unlike his
predecessor, Béchamp, he never published any of his works in major scientific journals but did
write about 500 articles that he published personally. He did not discount the fact that many
diseases came as a result of infection by external pathogens but added and extended the
Béchamp concept of disease coming from within the body. Although he lived until 1968,
Enderlein used primarily dark field examination of the blood but he did use the electron
microscope on occasions and was aware of scientific advances in microscopic techniques (such
as phase contrast) for living blood but did not extend his findings to the use of these
techniques.
However, Enderlein did accomplish several things:
He was to be the first to discover that bacteria have a nucleus but never credited with
the discovery because he didn’t publish the results of his work in credible scientific
journals.
He offered proof that the pH of the milieu was a major determining factor in the disease
process.
He offered proof that the blood is not a sterile environment (as was proposed by
Pasteur).
He proved Béchamp’s theory that the milieu (particularly the blood pH) was a most
important factor in determining the state of health of an individual.
He formulated treatment protocols based on isopathy – the Sanum products - based on
his ability to isolate and culture both the fungal forms of his symbionts from ferments
of the blood.
Many practitioners adhere to the teachings of Enderlein and regard dark field blood
microscopy as the pinnacle of Live Blood Microscopy and they look upon the success of
his Sanum products in the treatment of disease to be proof of his theory of disease.
Bradford (18) describes the Sanum products as inoculants made up of cell wall, cell
membrane, and other fragments from the various endobionts and other microorganisms
cultured from blood. As such their action would be to allow the immune system to build up
antibodies against the infecting microorganism(s) and, thereby, fight infection and disease
caused by the microorganism. However, that is not, in fact, what Sanum products are. They
are isopathic preparations of various forms of the symbionts and cell wall and membrane
fragments of microorganisms. What Enderlein describes as endobiont (Mucor racemosis
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Fresen) and Apergillus niger has led to his theories which, in turn, led to the development
of Sanum products which have proven most effective for the treatment of many health
problems associated with the upward development of these (and other) microorganisms in
humans.
Following on from Enderlein’s work on pH of the milieu, Dr. Robert Young based his
entire theory on the health status of an individual being due to changes in body pH and
promoted the concept of alkalization. He also has a considerable number of devotees to his
New Biology Live Blood microscopy in which he uses phase contrast. Much of the
microscopy ‘developed’ by Young was taken directly from Bradford’s HRBM® technique
but many of the interpretations have been altered and are out of context with published data
and my clinical observations on over 12,000 patients.
Hoekstra uses dark field microscopy in his Hemaview while Bradford uses a combination
of phase contrast, dark field and ‘pseudo differential interference’ microscopy in his
HRBM® blood test. Both rely largely on published scientific data to draw their conclusions
as to how one can interpret observed changes in the morphology of blood cells and other
blood elements. Bradford and Hoekstra both adhere to the medically accepted origin of
microorganisms but Bradford also recognizes the importance of all of the other factors that
influence our state of health (immune competence, homeostasis, pH, mind, spirit, oxidative
stress, etc).
2. Do candida spp. exist in the blood of ‘healthy’ individuals?
According to mainstream medicine Candida albicans is only found in the blood of

individuals who are chronically and/or terminally ill where it has been identified by
microscopy, culturing, and PCR techniques. Candida albicans has been linked with
superficial skin infections, oral and vaginal thrush, broncho-pulmonary infections,
secondary intestinal infections, scepticaemia, deep blood-borne infections such as
meningitis, endocarditis and pyelonephritis but according to orthodox medicine, is never
found in the blood of healthy individuals. C. Albicans, and other candida spp exist in the
mouth, nose, throat, intestines, vagina, and skin of man and under ‘normal’ circumstances
are non-infectious. However, if the immune system becomes compromised (eg in HIV or
other infections, iron-deficiency anaemia, certain cancers, or certain physiological changes)
candida can change to a fungal form and cause infection (both primary and secondary) of
its own. Some of the factors known to compromise the immune system and lead to candida
infections include diabetes, leukemia, iron-deficiency anaemia, neonatal debility, senility,
alcoholism, drug addiction, antibiotic therapy and cortisone therapy. Candida can exist in
humans as the yeast bud forms (in which case it seems to be relatively harmless to the
individual) but under certain physiological conditions (changes in pH, body temperature, or
in the presence of blood serum) it can change from the bud form to a more sinister ‘hyphal’
form which is pathogenic. Candida may also form psuedohyphae which are composed of
chains of elongated cells which have begun to grow into ‘hyphae’.
Since phase contrast microscopy has been used for the observation of live blood, white
round to oval shaped elements of around 2 – 4µ have been noted in the blood of patients
54
who were not considered to be unhealthy. Noting this, Bradford examined the white ‘buds’
over a time period and observed them change shape, budding off and producing hyphae-
like projections which then also budded off to form more of the white ‘buds’. He guessed
that these white ‘buds’ were Candida albicans and their presence in the blood indicated
some degree of candidiasis. Hoekstra, taking the orthodox position, disagreed that they
were candida and argued that they were platelet vesicles. However, Hoekstra only used
dark field and the candida buds are barely visible under dark field although they are starkly
visible in phase contrast. In 1995, Majid Ali and Bradford (3) used specific
immunostaining techniques combined with fluorescence microscopy to identify the white
‘buds’ as Candida albicans. Although their work was not absolute proof that the
microorganism was candida albicans it was adequate to satisfy many of their knockers that
candida spp. can be found in the blood of individuals who are not terminally ill.
Other workers (147) have also identified candida spp. in blood of ‘healthy’ individuals and
it is possible that it is these various forms (buds, hyphae, budding fungal forms) that make
up some of the structures described and noted by Enderlein during his examination of the
blood. These structures, however, certainly do not explain all of the elements that Enderlein
described and noted.
From my observations of blood taken from many thousands of patients with a very diverse
range of health problems and varying degrees of health status it would appear that each of
the ‘camps’ of Live Blood Microscopy have something to offer but none of them have the
complete answer when it comes to allocating indications to microscopic observations of the
morphology of blood cells and other blood elements. Bradford’s HRBM® test would be
the most comprehensive of these live blood microscopy tests (because it uses phase
contrast as well as dark field) but, due to the fact that it discards, out of hand, the work of
Enderlein and others it certainly is not complete. Many of the structures in the blood
described by Enderlein are readily observed and are not artifacts but the scientific
community has not taken it upon themselves to isolate and identify these structures.
Meanwhile, we know that observing the various symbiont structures in the blood can allow
the patient to be effectively treated by re-establishing ideal body pH and using the
appropriate Sanum preparation(s).
X. DARK FIELD LIVE BLOOD MICROSCOPY

DFLBM is a haematological screening technique developed, primarily, by Bradford Research
Institute (the High Resolution Blood Morphology [HRBM®] blood test), Hoekstra (the Hemaview
dark field blood microscopy test), and Enderlein plus my own clinical observations on over 12,000
patients. These tests allow practitioners to screen a fresh ‘wet’ blood smear for morphological
changes to blood cells and other blood elements using dark field microscopy. In the more powerful
live blood morphology test (LBM) phase contrast and pseudo differential interference microscopy
are also used in order to see more elements in the blood and allow better identification of these
elements.
Dark field microscopy is a commonly used technique for haematological studies in which the light
from the microscope is diffracted from the microscope objectives in such a way as to produce a
55
bright reflected image of solid objects (blood cells, crystals, etc.) against a dark background.
Crystals and crystalline materials in the cytoplasm of cells (such as in granular leucocytes) show up
as bright, glowing objects against this dark background. Dark field microscopy can allow the
observation of minute, low-contrast objects and transparent crystalline structures which are virtually
invisible under standard bright field microscopy.
In DFLBM dark field is used exclusively and, therefore, some valuable information about the
patient is lost.
It should, again, be noted that DFLBM is not a diagnostic procedure as used by clinical pathology
laboratories and is not advocated for use as such but it is an excellent screening tool for gaining a
great deal of knowledge about the patient's general health and well-being and is an important
screening device for use in the individualised, integrated, metabolic approach to health therapy.
Although DFLBM is not a classical diagnostic procedure it enables the practitioner to get a holistic
view of the patient's individual nutritional status, body organ functions, bone marrow activity,
immune system function, and much more. Unlike some other techniques, LBA gives us an accurate
insight into what is currently happening in the body now and, as such, allows us to offer true
preventive care to patients. It is in many ways equivalent to several of the other techniques combined
but also works wonderfully well in conjunction with other natural therapy diagnostic techniques
such as the Coagulated Blood Morphology test, Eye Diagnosis, Urine Analysis, and
Symptomatology and Diagnosis. With this in mind, it must be stated that much of the interpretation
of blood observations through LBA is based on solid haematology as studied at medical schools in
universities in addition to empirical knowledge.
From observations made on the blood using DFLBM the practitioner is able to formulate a
customised nutritional programme (diet), Sanum therapy, and supplementation with vitamins and
minerals, herbs, etc. all of which is specifically geared to the individual needs of the patient and
designed to assist in the restoration of their health and well-being.
1. Blood Collection
a. All equipment necessary for both blood collection and microscopy must be ready prior to taking
a blood sample. The blood collected will only be in an active 'live blood' state for approximately
15 to 20 minutes from time of collection so it is important to avoid any time delays where
possible. The equipment needed for collection includes clean slides, cover slips, lancets, alcohol
wipes, and clean tissues. The glass slides often come with some dust and fine particles smeared
on them from the supplier so it is a good idea to scrub each slide thoroughly with a Kim Wipe
then touch the slide with a clean metal object (eg a metal pen) prior to blood collection to remove
electrostatic charge from the slide. Report forms should also be filled in with the patient's details
ready for recording microscopic observations. The microscope and all ancillary equipment
attached to it (monitor, video camera, computer, and printer) should be switched on and the date
set accordingly. Settings on the microscope for initial (eyepiece viewing) observations are dark
field setting and X20 objective.
b. Make the patient comfortable and ask them to hold out their hand. For consistency and
56
comparison of data collected, it is preferred that the index finger of the left (or the right) hand is
used every time.
c. Clean the patient's finger thoroughly with an alcohol wipe and then dry thoroughly using a clean
Kim-Wipe tissue. It is important to remove all alcohol from the finger so as to avoid any possible
damage to blood cells from this source.
d. While holding the patient's finger between your finger and thumb, roll your thumb toward the
tip of the finger to make sure the end of the finger is taught and continue to apply slight pressure
to the finger using your thumb around the first joint of the finger. Remove the sealed cap from
the end of the lancet and, while holding the lancet perpendicular to the fingerprint lines, apply
enough pressure to just break the skin with the lancet. Use a single swift movement so as to not
stress the patient by taking too long. Continue to apply pressure to the first joint of the finger to
express enough blood so that a neat drop about 1.5 - 2 mm in diameter is on the skin. Quickly
pick up the plain slide you have ready for the DFLBM and lower it onto the drop of blood so
that it just touches the drop. Do not let it touch the skin! Lift the slide with the small drop of
blood on it and immediately cover with a cover slip. The blood should spread easily to form a
thin layer which is the thickness of single blood cells. If the blood does not spread immediately
the cover slip is placed on the slide, lightly tap the top of the cover slip with a metal biro or pencil
so that the blood forms a nice single layer of cells between the slide and the cover slip. The blood
sample is then ready for DFLBM microscopic examination.
2. Microscopy
View the blood through the eyepieces (using X20 objective and dark field) and scan the slide to get
an overall estimate of the general state of the blood. While scanning count the number of white
blood cell in about 5 to 10 fields of view then divide the total by the number of fields you counted
to get a rough estimate of white blood cell numbers. A count of approximately 10 to 15 per field is
normal at this magnification. Don't forget to count all white blood cells - granular and agranular
leucocytes. While scanning, note if there are any unusual cells, abnormal cells, excessive amounts
of crystals, platelet aggregates, red blood cell aggregates, etc.. When you are happy that you have a
good overview of the blood select an area which is most representative of the overview, which
contains any specific cells/crystals, etc. that you wish to show the patient and move to X40
objective, refocus, and transfer the image to the screen of the monitor for detailed viewing. While
you are viewing the blood on the screen discuss briefly with the patient what the observations
indicate and get some feed-back from the patient. Continue to discuss observations with the
patient while making notes on the DFLBM form of all observations and their magnitude. When
you jhave completed examination of the blood at 40X objective and discussed all indications with
your patient you can place drop of immersion oil on top of the slide and use the 100X dark field
objective to examine the blood – mainly to observe Enderlein structures. Again discuss all of your
findings with the patient and get their feedback so that you can make an educated diagnosis from
the information the patient give syou regarding their symptoms, signs, and feedback from the
possible indicators for observation you have made on their live blood.
57
Remember that the blood will dry out with time and that the blood is an ideal medium to support
the growth of microorganisms so try to finish all microscopy on the live blood sample within about
15 - 20 minutes.
From the observations impress upon the patient the need to follow strict dietary and nutrition
guidelines plus taking appropriate Sanum products you arrange for them in order to help them
overcome their health problems and also get the message across that when they come back for a
follow up visit that improvements will only be noted if they strictly follow those organized
guidelines. Cheating will often result in less noticeable improvements on their part. In other words
they will be caught out!
3. Observations and Recommendations
a. Normal, healthy blood
i.Erythrocytes
Erythrocytes in healthy blood are generally round, of uniform diameter, bi-concave in shape, and
well separated or, at least, only just touching one another. Under dark field they appear as bright
circles while under phase contrast they appear as donuts with a white centre with a bright 'halo'
around the cell membrane. Under differential interference the rbc’s appear as biconcave discs. The
bi-concave shape of the erythrocyte is due to the interaction of contractile proteins (spectrin, actin,
protein 4.1, and ankyrin) that exist on the internal side of the red blood cell membrane.
58
ii. Neutrophils
Active neutrophils will exhibit moving granules in the cytoplasm and constantly changing shape as
they move slowly through the plasma. They are noted by their many (3-5) lobed nucleus and fine
cytoplasmic granules.
iii. Eosinophils
Eosinophils, like neutrophils exhibit streaming cytoplasmic granules and constantly changing shape
when active. They are notable by the large, granular deposits in the cytoplasm (which fluoresce with
a bright white glow under dark field) and a bi-lobed nucleus.
59
iv. Basophils
These are infrequently seen in the blood picture but are notable by their very large, non-fluorescent,
granules in the cytoplasm and clover-leaf shaped nucleus.
Enderlein never described eosinophils or basophils in his work but did note the presence of white
blood cells with dense granules in the cytoplasm in the blood that he described as “leucocytic plasma
invasion”. He argued that the granules were symprotits, sporoid symprotits, or microthrombocytes.
Enderlein associated these white cells with Hodgkin’s lymphoma and lymphocytic leukaemia.
v. Monocytes
These cells are slightly larger than the lymphocytes and smaller than the neutrophils. They have a
quite distinct U-shaped or kidney-shaped nucleus.
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vi. Lymphocytes
T-Cell
B-Cell
These are the smallest of the white blood cells and are distinguished by their single, round nucleus.
In T-Cells, the nucleus fills most of the cytoplasm. They are round to slightly oval shaped cells. In
B-Cells the nucleus only fills about ¹/3 to ½ of the cytoplasm. T-cells and B-cells are mostly
approximately the same size as large erythrocytes but B-cells can often be about 50% larger than
rbc’s (eg. during allergic reactions). Under certain conditions (eg. viral infections) the T-cells can
also be greatly enlarged so it is erroneous to tell them apart based on their relative size.
vii.Phagocytic Macrophages
Phagocytic macrophages are the 'Pac-Men' of the blood, destroying and ingesting foreign particles
including bacteria. They are slightly larger than normal monocytes and usually contain a lot of
ingested material in cytoplasmic vacuoles. These cells are rarely seen in normal blood but can
appear in cases of acute infection.
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viii. Platelets
Platelets appear as small discs approximately 2µ in diameter (less than one third the size of an
erythrocyte). Unfortunately they are not easily visible under dark field. They are well dispersed
throughout the blood. Although non-motile, they may sometimes appear active due to Brownian
movement through external light stimulation. Sometimes the platelets may be seen to be elongated
and may even have what appear as fine threads attached to them. Emderlein described these as
abnormal thrombocytes and the disc shaped ones as normal thrombocytes. Enderlein also indicated
that thrombocytes contained nuclei and that they were produced as a result of division of the nucleus
of the Cystit. Haemotology texts describe the origin of thrombocytes as being the bone marrow via
the blast cells called megakaryocytes. They are essential for well being and are involved in the
coagulation process. If platelets aggregate it can indicate a number of possible problems mostly
associated with poor diet but this is also seen commonly in the peripheral blood of patients who
have thrombocythaemia, in which case they are producing excessive numbers of thrombocytes and
is a sign of hyperplasia of the bone marrow. It often accompanies other myeloproliferative diseases
such as polycythaemia, myelofibriosis, and acute myeloid and lymphoblastic leukaemias. These are
all associated with stem cell-based disorders.
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b. Abnormal Red Cell Observations
i. Protein Linkage
Protein linkage is observed as red blood cells adhering to one another through a single point of
attachment. Their physical appearance is one of lemon-shaped cells joined at the pointed ends.
Several red blood cells can link up in this manner giving the appearance of linked 'chains' of cells.
Linkage is due to an imbalance in the cell membrane surface charge due to changes in blood pH
which results primarily from poor protein digestion but may also be an indication of an alkaline
blood profile. Treatment of these conditions is by the administration of betaine hydrochloride,
glutamine hydrochloride, pepsin, gentian root, and vitamin B3. Betaine and glutamine
hydrochloride provide additional hydrochloric acid to the stomach, pepsin assists in enzymic
digestion of proteins in the stomach, and gentian root stimulates the parietal cells to produce more
hydrochloric acid. Protein linkage is also indicative of an alkaline blood profile so it is important to
ensure that the patient is placed on a diet which is high in the low protein, acid-forming foods such
as pasta, breads, asparagus, Brussels sprouts, lentils, artichokes, etc. If protein linkage is not arrested
by nutritional intervention the blood cells may become more 'sticky' and rouleaux can result. Other
possible health problems associated with protein linkage include: myelophthistic anaemia and
myelofibrosis. Enderlein also related protein linkage to hyperproteinaemia but additionally linked
this phenomenon with the presence of higher valence forms of Mucor racemosus in blood.
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ii. Rouleaux Formation
A number of physiological factors can cause red blood cells to stick on top of each other forming
what appears as 'stacks of coins'. This blood cell formation is known as rouleaux. Factors which
cause rouleau include: poor digestion/assimilation of proteins and/or fats, hyperproteinemia (106),
reduced oxygen transport in the lungs, fatigue, lethargy, multiple myeloma, temporal arteritis,
polymyalgia rheumatica, other collagen vascular disorders, and asthma. The degree of rouleaux
formation is directly proportional to the amount of asymmetric protein molecules found in the
blood. These proteins adhere to the surface membranes of red blood cells which then undergo a
change in their surface charge from negative to positive. Positively charged cells are then attracted
(and adhere) to cells which have not been coated with asymmetric proteins thus forming the
rouleaux. When erythrocytes rouleaux the surface area of rouleaux’ed cells is greatly reduced and
thus their oxygen absorption from the lungs is greatly reduced. A reduction in oxygen carrying
capacity of these cells leads to a reduced respiration rate in the mitochondria which, in turn, leads
to a reduction in ATP production. Consequently, patients exhibiting a considerable degree of
rouleaux tend to fatigue easily (run out of stored energy), are lethargic, and probably show
tendencies toward muscle weakness or tightness. In rouleaux the red blood cells tend to retain their
normal biconcave shape. Enderlein also argued that rouleaux was a sign of hyperproteinaemia along
with lemon-shaped (protein linkage) and pear-shaped (teardrop) red blood cells and the viscous
movement of blood cells. If left standing the blood has a tendency toward the formation of long
thread forms (chondrits) and rod forms (ascits). The presence of erythrocyte symplasts (rouleaux,
rbc aggregation) and protein crystals in the blood were also indicative of hyperpoteinaemia.
Treatment of patients with rouleaux is primarily with digestive enzymes (trypsin, chymotrypsin,
and lipase), pepsin, hydrochloric acid (as above), and vitamin B3, all of which will lead to an
increased breakdown and metabolism of proteins and fats. To assist this process the diet must be
altered to eliminate saturated fats and reduce intake of high density protein foods such as red meats,
poultry, and eggs but increase intake of fibre and complex carbohydrates. Treatment with Sanum
would involve initially using Alkala-N to alkalise the milieu followed by Sanuvis and Citrokehl.
This would be followed up with Mucokehl.
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If the slide is tapped under the microscope rouleaux formation is often broken and the cells will
momentarily dissociate only to re-associate again. This is a simple test to differentiate between
rouleaux and red cell aggregation if you are unsure.
iii. Erythrocyte aggregation
Aggregation of red blood cells is a more serious observation than rouleau as the oxygen-carrying
capacity of the erythrocytes is greatly reduced and blood flow through capillaries is significantly
reduced. This means that insufficient oxygen and nutrients are carried to peripheral cells in the body
and insufficient toxins are removed from these peripheral cells. The body thus becomes toxic and,
in extreme cases, aggregation may even lead to clot formation which increases the person's chances
of stroke. Agitation of the slide by tapping with a pen or pencil will not break up red cell aggregates.
The red cells also often appear misshapen, particularly around the perimeter of aggregates.
Acute-phase proteins increase in the blood plasma in response to cell damage and toxin
accumulation and these acute-phase proteins assist in aggregation of red blood cells. High blood
fats and lipoproteins plus systemic reactive oxygen toxic species (ROS) have also been associated
with increased aggregation of erythrocytes.
Smoking can cause aggregation of erythrocytes due to carbon monoxide in the cigarette smoke. The
carbon monoxide binds irreversibly with haemoglobin thus displacing oxygen from the red blood
cells and preventing oxygen uptake. High caffeine intake, emphysema, chronic or degenerative
conditions, severe allergies, and poor calcium/phosphorus balance can all contribute to erythrocyte
aggregation.
Enderlein called these red blood cell aggregates erythrocyte symplasts and looked upon them as a
progression of sclerosis or congestion of lymph tracts and vessels.
Treatment of aggregation of erythrocytes is similar to that for rouleaux with the additional
supplementation of essential phospholipids (lecithin), essential fatty acids (particularly omega-3
fatty acids), and extra vitamin B3 (as nicotinic acid). Vitamin E and vitamin C supplementation also
help to break up aggregates. In extreme cases EDTA-chelation therapy can be effective in breaking
up aggregates.
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iv. Anisocytosis
Anisocytosis refers to any condition in which the erythrocyes exhibit obvious variations in size. It
is present to some degree in most cases of anaemia. It may also be attributed to the over-production
of cortisol from the adrenal glands during emotional stress. However, this can lead to an inhibition
of the enzyme methyltetrahydrofolate reductase which, in turn, leads to deficiencies in folate. Most
often this is noted in depression in the elderly and it is expressed in the blood as the presence of
macrocytes (see below).
(1).Microcytes
Red blood cells smaller than normal (microcytes) have a lower than normal haemoglobin content
and are seen if a person is anaemic, during menses, poor iron assimilation, or if there is a problem
with bone marrow function. Microcytosis is indicative of low iron or folate status and certain genetic
defects associated with abnormal haemoglobins (6, 22).
Treatment is to provide the patient with an iron supplement. Vitamin C assists with iron absorption
and it is also important that the stomach is producing enough acid so that the iron is in its ferrous
form which is the most readily absorbed form of iron.
(2).Macrocytes
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Macrocytes are blood cells that are larger than normal and are indicative of primarily a deficiency
in vitamin B12 and/or folic acid. Pernicious anaemia is one instance when you commonly see a
number of macrocytes in the blood. Haemolytic anaemia also leads to excess production of
macrocytes. Other factors which can contribute to macrocyte production include menses, poor
calcium/phosphorus balance, and deficiencies in zinc, selenium and vitamins A, C, E, and B6.
Macrocytosis is also associated with low B12 or folate status and liver disease (86) and
hypothyroidism (149).
Treatment consists of providing the patient with a supplement which is high in vitamins B12, B6,
C, A, and folic acid plus iron.
v.Poikilocytosis
Poikilocytosis refers to any condition in which the erythrocytes exhibit obvious variation in shape
from their normal biconcave shape. Cells may be oval, pear-shaped, teardrop-shaped, pencil-
shaped, or irregularly shaped such as bottle-top, helmet, triangular, flattened, torn, or burred, shapes.
The term which describes all red blood cell fragments is schistocytes. When schistocytes are present
it is an indication that haemolysis is taking place. Schistocytes are present to a minor scale during
menses, are more common during haemolytic and megaloblastic anaemia, and are common
following severe burns. As poikilocytosis is largely due to damage to red blood cell membranes the
presence of toxins in the blood can cause an increase in the presence of odd shaped erythrocytes.
These toxins may be produced through digestive problems such as leaky gut syndrome (dysbiosis),
poor liver function (poor elimination of toxins), or due to reactive oxygen species (ROS). Rbc’s that
have the appearance of a ‘chunk’ cut out of them (bite cells) are usually indicators of excess lipid
peroxidase activity and would suggest that the patient needs treatment with potent antioxidants
(particularly vitamin E). Certain pharmaceutical drugs can also lyse red blood cells causing
poikilocytosis so it is important to ask your patient if they are taking any prescribed drugs and
consult your MIMS (or other drug guide) to establish whether drugs may be contributing to the
condition. Illicit drugs may also contribute to poikilocytosis. Some of the drugs which are known
to cause haemolysis of blood cells include solazapyrin, some NSAIDS, and chemotherapeutic
agents such as methotrexate which is commonly used in the treatment of rheumatoid arthritis.
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Another factor that leads to poikilocytosis is alterations in the level and activity of spectrin and
elastin proteins in the cell membranes (see earlier). The activity of these proteins is affected by
changes in the cholesterol/phospholipid ratio in the cell membrane. For example, acanthocytes
(bottle tops) may be formed as a result of elevated blood cholesterol levels. According to Enderlein
the presence of any red blood cell deformity in the blood is an indication of acute illness.
(1).Pencil cells
Pencil cells are very thin, elongated, erythrocytes and appear during anaemia, particularly
haemolytic anaemia. They may be the result of certain mineral and trace element deficiencies
(particularly those involved with scavenging free radicals (copper, zinc, manganese, iron, and
selenium) or bone marrow problems such as myelofibrosis.
Treatment is by supplementation with a well balanced multivitamin, multi-mineral, formula which

contains iron, magnesium, calcium, zinc, copper, manganese, plus vitamins C, A, and all of the B-
group.
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(2).Elliptocytes or Ovalocytes
Oval-shaped erythrocytes are known as elliptocytes and they may be present in the blood under
several conditions. Some individuals have a genetic disorder which leads to up to 80 - 90% of their
erythrocytes exhibiting elliptocytosis. Elliptocytes are also seen to a lesser degree in healthy patients
(up to 10%) but may increase in number during radiation therapy, chemotherapy, all types of iron
deficiency anaemia, or magnesium deficiency. One possible factor that leads to the formation of
elliptocytes is defective spectrin-polymer formation and band 4.1 proteins in the red blood cell
membrane (148).
Treatment is with magnesium, iron, and multi-vitamins as for the presence of pencil cells in the
blood.
(3).Acanthocytes - membrane damage/bottle tops
As mentioned above these are seen under a number of conditions including haemolytic or
megaloblastic anaemia but may also be present to some degree during environmental or chemical
allergies, virus activity (Epstein-BarrVirus or Cytomegalovirus, in particular), oxidative stress, poor
liver or spleen function, splenectomy, hepatitis, cirrhosis, or yeast infections such as candida. It is
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also possible that slowed cholesterol metabolism or elevated serum cholesterol may cause higher
than normal cholesterol concentrations in the red cell membrane which, in turn, leads to acanthocyte
formation. Acanthocytosis is associated with anaemia, oxidative stress, and liver disease (39, 80).
Enderlein’s interpretation of the presence of these structures in the blood is that they are an
indication of the rise in valence of the endobiont to increasing pathogenicity. He believed that
acanthoctytes were a precursor of the ascit phase.
Treatment: In addition to providing the patient with all necessary vitamins and minerals to support
blood cell production it is also important to treat which ever condition may also be contributing to
damage of the red cell membranes. The use of Sanum remedies such as Alkala, Mucokehl, Pinikehl,
and Sanuvis can reverse the progression to the ascit phase and reduce acanthocye formation.
(4).Spiked/crenated/shadow red blood cells – Echinocytes
These structures are extreme or advanced forms of acanthocytes and are mostly associated with
high levels of oxidative stress. The presence of echinocytes (spiked red blood cells), burr cells, or
ghost cells (shadow cells) indicates a chronic or degenerative condition and is often accompanied
with muscle soreness and/or fatigue. Virus activity, chemotherapy, radiation therapy, and chronic
fatigue syndrome are just some of the situations which can lead to this condition of the blood. Often
the patient is very low in minerals such as magnesium, chromium, selenium, and/or zinc.
Magnesium deficiency increases lipid peroxidation which in turn leads to echinocyte formation
(54). Albumin deficiency caused by poor absorption of amino acids across the gut wall, poor intake
of dietary proteins, or poor digestion of proteins can also lead to crenation of red blood cells (81).
Certain vanadium salts can lead to defects in the band 3 proteins in the red cell membrane resulting
in the formation of echinocytes (16). One source of these vanadium salts is black pepper, so
excessive intake of black pepper may lead to excessive echinocytes in the blood (115).
Enderlein described these elements as dioecothecits and their presence in the blood was a sign of a
good ‘defensive system’, although the presence of a large number of them was a “wake up call that
should not be ignored”.
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Treatment is similar to that for pencil cells with extra emphasis on whichever vitamin or mineral
deficiencies are noted in the blood analysis plus specific treatment of any known disorder, with
particular emphasis on antioxidant supplementation.
v. Hypochromic red blood cells
Hypochromic erythrocytes are noted as having a much larger than normal centre indicating that
they are extremely biconcave in shape. They are not easily seen under dark field but are obvious
under phase contrast. These cells are low in haemoglobin and indicative of anaemia.
Treatment is as for other forms of iron- deficiency anaemia.
vi. Rbc inclusion bodies
(a) Rbc dots
(b) Rbc inclusions
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Erythrocytes with ‘white’ dots inside an indication of external microorganisms ‘parasitising’ the
red blood cell such as in cases of toxoplasmosis. If the ‘white’ dots are moving and have a dark spot
in the centre they are most likely mycoplasmas. Other inclusion bodies are possibly cell wall
deficient forms of bacteria or yeasts. Enderlein interpreted these inclusions to be the result of the
high valence endobiont reaching the bascit form from the Mucor racemosus cyclode as a result of
disturbances in the milieu, or terrain. Whatever the explaination, inclusions are associated with
immune dysfunction and/or increasing pathogenicity.
Treatment includes supplementation with colostrum and zinc to boost the immune system while
eating alkaline foods is highly recommended.
vii. Rbc patterns, crescents
Odd shaped white pattern or crescent-shaped patterns in the red blood cells are consistent with
microbial infections and may also be present if the patient suffers from severe headaches or
migraine. These bodies are also, most likely, mycoplasmas.
Treatment is to use Sanum therapy for mycoplasma infections or treat with specific radio
frequencies using a frequency synthesizer device. Modulating the immune system with colostrum,
zinc, vitamin C, etc. plus Sanum products such as Utilin, S-Utilin, Recarcin, Rebas, etc. would be
of great benefit.
For migraine headaches it is important to supplement with high doses of magnesium and, if
indicated, establish food allergies which may contribute to the migraine/headache. Avoidance of
food allergies can frequently eliminate migraines. Other factors which can trigger
migraine/headaches include trauma to neck, shoulders or back. If this is indicated specific massage
and/or chiropractic adjustment is required.
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viii.Target Cells
Target cells appear as ‘normal’ shaped cells but they are not truly biconcave in shape. They appear
as concentric rings (a target) under phase contrast but are not as obvious under dark field. One factor
contributing to this shape change is an increased level of both cholesterol and phospholipids in the
red blood cell membrane. Target cells can also be the result of anaemia (80) and liver disease (39).
Enderlein argued that target cells (codocytes) were an indicator of increasing development of the
endobiont to a pre-emerging stage in which the annulus is described as an inclusion in the red cell
resulting from a disturbance in the milieu due to dysbiosis, including hepatoportal pathways. In
most instances target cells are always accompanied by some form of anaemia.
ix. Spherocytes
Spherocytosis is a genetic disorder that leads to the production of spherical shaped red blood cells
and may be due to either a defect in spectrin production or a decrease in spectrin production in the
red blood cell membrane. These cells are not discernable from normal red blood cells under dark
field examination but may be seen under pseudo differential interference and phase contrast
microscopy.
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x. Schistocytes, Bite cells
Red blood cell fragments are due to damage to rbc’s by contact with abnormal surfaces (eg artificial
heart valve, arterial grafts, stents etc) or as microangiopathic haemolytic anemia caused by rbc’s
passing through differential intravascular coagulation (DIC) present in small blood vessels or
damaged small vessels in malignant hypertension, haemolytic uremic syndrome, thrombotic
thrombocytopenic purpura, pre-eclampsia, or meningococcal sepsis. Rbc fragments have been
demonstrated to be associated with chronic glutathione depletion (78) and haemolytic anaemia
associated with long-standing diabetes mellitus (21).
Enderlein argued that any red blood cell deformities were an indication of acute illness.
Treatment protocols would involve the use of potent antioxidant formulas (vitamins C, E, A, B1,
bioflavenoids, carotenoids, glutathione, cysteine, and sulfurofane) along with the required co-
factors (selenium, iron, copper, zinc, and manganese).
c. Abnormal White Blood Cell Observations
i.Wbc's fewer than normal (leukopenia)
A decrease in the number of white blood cells is consistent with a suppressed immune system and/or
bacterial infection. The low numbers of leucocytes has been shown in patients with HIV (71) and
those under-going chemotherapy (55, 58).
Treatment is to improve the diet and make sure that lots of fresh fruits and vegetables are eaten,
plenty of good quality water is consumed, and to supplement with vitamin C, B-group vitamins,
zinc, manganese, copper, and herbs such as Echinacea, garlic and thyme.
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ii.Wbc's more than normal
Increased numbers of white blood cells are seen during viral (lymphocytes) or yeast infections
(granular leucocytes) and certain types of leukemia (blasts). They frequently appear as aggregates
of neutrophils. Excessive leucocytes have been demonstrated in lung infections (109) and patients
who have undergone blood transfusions (52).
Enderlein described these aggregates as sclerosymprotit symplasts and were an indication of
progressive sclerosis or congestion of the lymph tracts and vessels.
Treatment is as for decreased white blood cell numbers (above).
iii.Neutrophils too few, granules inactive
White cell viability is extremely important to a healthy immune system. The PMN's should exhibit
movement of cytoplasmic contents and overall movement of the whole blood cells as they move
through the plasma in their role as phagocytes. In the ideal case around 75%, or more, of the PMN's
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should be active. Less than 50% activity of these cells would be considered poor and indicate that
the immune system is being suppressed by some factor such as an acute infection, exposure to toxic
chemical agents, or hereditary factors. Inactive PMNs correlate with weak immune activity or
taurine deficiency (53). They also are associated with low B12 and/or folate levels (145),
chemotherapy (87), and radiation therapy (165).
Enderlein argued that inactive leucocytes were a sign of more serious infections, intoxication from
heavy metals or pharmaceutoical drugs, or the influence of geopathies or electromagnetic pollution.
Treatment is as for decreased wbc numbers (as above).
iv.Neutrophils hypersegmented
Normal PMN's contain approximately 2 to 5 lobes of their nucleus with the average being 3 lobes.
During acute infections, especially those due to cocci bacteria, spirochetes, viruses, or parasites;
environmental or chemical poisoning (such as lead, mercury, illicit drugs, digitalis, epinephedrine,
and insect venoms); the PMN's can become hypersegmented and more than 5 lobes will be seen on
the nucleus. The hypersegmented PMN's are also greatly increased in the presence of rapidly
growing neoplasms; especially those in the liver, bone marrow, or gastrointestinal tract.
Hypersegmanted neutrophils are correlated with vitamin b12 and folate deficiency, chemotherapy,
radiation therapy, anaemia, and infections (87).
Treatment protocol is as above for immune system support/stimulation and/or treatment of specific
contributory conditions such as gastrointestinal tract, liver, etc.
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v.Neutrophils irregular, fragile
If the white blood cells appear fragile, inactive, and have irregular shape it suggests a chronic
condition or problem with blood cell production at the bone marrow.
Treatment is to boost blood cell production by supplementing with a very good multivitamin/multi-
mineral formula which contains iron, magnesium, zinc, copper, manganese, vitamins C, A, E, B6,
B12, folic acid, etc. and ensuring that the diet consists of mainly fresh fruits, vegetables, vegetable
juices, fish, lean meats, broths, and soups.
vi. Eosinophils excessive
An increase in eosinophil numbers from around 1 - 2% of the white blood cells to greater than 2%
is indicative of mostly allergy problems (IgE and IgG) and/or infections with yeasts or parasites.
However, lung problems, chemotherapy damage, Hodgkin’s disease and detoxification from
prescription drugs can also lead to eosinophilia. Excess eosinophils correlated with intestinal
parasites, allergies (146), traumas, respiratory problems (57), plus endocardial and microvascular
damage to the heart or respiratory system (50).
Treatment protocols will vary according to the cause(s) of the problem. If allergies are indicated
allergy tests may be necessary to establish which allergens are causing the problem and to take
appropriate action. If parasites are indicated, treatment to eliminate the parasites is obviously
appropriate.
vii. Basophils excessive
Basophils are histamine-containing granulocytes which are increased in number during any allergy
reaction but are mostly associated with environmental allergies such as pollens, grasses, chemicals,
perfumes, dust, house mites, etc.. The presence of greater than 1% basophils in the white blood cell
population can also be associated with hives, rashes, palpitations, attacks of flushing, diarrhoea,
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watery eyes, cataracts, dark circles around the eyes, and hay fever symptoms (runny nose, itches,
etc.).
Treatment is with high dose vitamin C, liver support formula, and high dose bioflavonoids (eg. from
citrus peels).
viii. Lymphocytes excessive (lymphocytosis)
Bacterial or viral infections (activated immune system) and environmental chemicals

are the main causative factors of elevated lymphocyte numbers. Leukaemic patients may also have
excess lymphocytes as well as large numbers of blasts in the blood. It is important to make sure that
you clearly distinguish between blasts and lymphocytes as they are very similar in size and shape.
Treatment is, again, as for (i), above.
ix. Lymphocytes low (lymphocytopenia)
Low lymphocyte count is observed in several immune-deficiency syndromes including AIDS

which may be due to destruction of the T-cells by the Human Immunodeficiency Virus (HIV) (71),
however, the fact that HIV is the only causative factor in AIDS is open to some conjecture.
Chemotherapy is also a major destroyer of lymphocytes (as well as other blood cells) and can lead
to decreased lymphocyte numbers (121). Other facors leading to low lymphocyte numbers include
exposure to lead, manganese, industrial solvents, and/or microwaves (93) and psoriasis (94).
Treatment is to boost and support the immune system by diet and supplements, as above.
x. Enlarged T-cells
During viral infection or other immune system activation T-cells become enlarged and may also
exhibit granular deposits in the cytoplasm. Some T-cell enlargement has been observed in cases of
severe inflammation such as arthritis attacks.
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Treatment is for viral infections, as above.
xi. Monocytes high
An increase in the numbers of monocytes above 4% of white blood cell numbers is indicative of
infection (particularly bacterial or viral) but also occurs with Hodgkin’s disease and in response to
protozoan or rickettsial infections and subacute bacterial endocarditis.
Treatment is as for all microbial infections.
xii. Macrophages high
Macrophage numbers greater than 3% of white blood cell population is indicative of immune
system activation, severe infection, lupus erythematosus, and haemolytic anaemia.
Treatment: It is important to design a treatment programme not only to boost and support the
immune system but also to treat the underlying causative condition.
xiii. Band neutrophils
If band neutrophils are present at greater than 3% of the white blood cell population it is suggestive
of acute trauma, blood loss, or severe inflammation such as in appendicitis.
Treatment protocols are to be tailored to the specific condition.
xiv. Blasts
Blast cells are immature red and/or white blood cells. Their appearance in the blood is always
associated with bone marrow problems and most often is associated with leukemia or lymphoma.
Enderlein believed that blasts were not nucleated but rather filled with endobiont chondrits/spemits
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which form a “pseudo-nucleus” however, modern staining techniques and PCR technologies have
firmly established the ‘nuclear’ material in blasts as DNA.
d.Abnormal Platelet Observations
NOTE: Platelets are not often easily seen under dark field examination and appear as faint small
circles about 1 – 2 µ in diameter. They are, however, very obvious under phase contrast.
i.Platelet aggregation
Platelets aggregate in response to a number of factors including platelet aggregation factor,

thrombin, collagen, ADP, excessive fats in the blood, thrombocytopaenia, and smoking. They
appear as small to large aggregates in LBA. Excessive aggregation can lead to thromboses (clot
formation) which can, in turn, lead to stokes and/or heart attacks. Enderlein called these
thrombocyte symplasts and believed that they were an indication of a progression of sclerosis or
congestion of the lymph tracts or vessels.
Treatment is to put the patient on a very low fat, high protein (fish, legumes, lentils,
poultry, lean meats), high fibre diet and to supplement with vitamin C, vitamin E, omega-3 fatty
acids, and lipotropic agents such as methionine, choline and inositol.
80
ii.Platelets surrounded by mucopolysaccharide material.
When platelets (either single or aggregated) are surrounded by a mass of mucopolysaccharides (pale
grey ‘halo’) it is an indication of the presence of gram negative bacteria (predominantly in the gut)
and possible vascular problems. Most often it indicates dysbiosis in the gut and resultant endotoxin
activity.
Bifidus and lactobacillus bacteria to re-colonize the gut plus Pau d’arco, Golden Seal, Burdock, and
other anti-bacterial herbs are recommended to reduce the amount of toxic bacteria.
e. Other observations:
i.Fats and fibrin
(1).Chylomicrons excess
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These are fat droplets from ingested animal fats, dairy products, etc. and/or oils from nuts, seeds,
margarines, etc. If present in excessive quantity they may merely indicate that the person has
recently eaten foods high in fat or oil content. If, however, they are present to excess in the blood
when that person has not eaten fatty or oily foods then it may indicate that the person may suffer
from hyperlipoproteinaemia. In that case the person concerned would be more prone to accelerated
coronary artery disease, atherosclerosis, liver and spleen enlargement, and glucose intolerance.
Treatment is to eliminate all saturated fats, fatty foods, fried foods, and polyunsaturated oils from
the diet allowing only essential fatty acids from flax seed, fish, and supplements such as omega-3
and omega-6 fatty acids to be included in the diet. Supplementation with 'soluble' fibre from oat,
barley, or rice bran and lipotropic agents such as choline lecithin, inositol, methionine, and carnitine
will also assist.
(2) Fibrin net.
Fibrin ‘spikules’ are composed fibrin proteins which take on the shape of long, needle-like
projections. These appear in the blood under situations of liver stress which can have several causes
including drug or alcohol abuse, dysbiosis (endotoxins), excess fat build-up, liver malfunction at
Phase I or Phase II of detoxification pathways, or exposure to toxic chemicals (exotoxins). Enderlein
saw rapid filament (fibrin) formation as an indicator of hyperacidity. It is often accompanied by red
blood cells with thick, bright (endobiont burdened) membranes with a high tendency for
degeneration. When left standing, the blood has a tendency for forming burr cells (acanthocytes),
echinocytes, and high valence macrosymprotits (mycoplasmas). Spikules have also been associated
with drug therapies such as chlorpromazine (124, 127).
Enderlein noted spikules as being fibrin and its presence in the blood was an indicator of upward
development of the endobiont in the Mucor cycle.
Treatment consists of boosting liver function with liver formulas which include methionine,
cysteine, cystine, B-group vitamins, liver extracts, high protein, low fat diet, and elimination of all
toxins, drugs, and chemical agents from the diet. Drinking sufficient water (2 litres) daily will also
help facilitate the flushing of existing toxins from the body.
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(3) Lipid Ribbons
Lipid ribbons appear as irregular, flat, ribbons of opaque material under phase contrast dark field.
The ribbons may be from as small as around 20µ up to at least 200µ in length. They are an indicator
of poor lipid digestion/metabolism, elevated cholesterol levels, and/or high fat diet. Lipid ribbons
and lipid plaque correlate with early stages of atherosclerosis or changed homeostasis (147, 153).
Enderlein called these filit-colloid symplasts which also indicated progression to sclerosis and
potential coronary heart disease.
Treatment is to put the patient on a non-sugar, low saturated fat, high soluble fibre diet such as the
Cretan diet and supplement their diet with omega-3 fatty acids, garlic, and anti-oxidants.
(4) Protoplasts
It is unclear as to what function protoplasts have but they are translucent, irregular shapes, varying
in size from small to quite large, and consisting of an aggregate of red crystals, cholesterol crystals,
other crystalline shapes, and possibly, platelets. They are most likely early indications of plaque
formation. Under dark field the crystals may fluoresce brightly and make it difficult to see the other
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elements in the protoplast. Some have different colours. Enderlein described protoplasts as
symplasts and psuedocrystals.
Treatment is a diet which avoids saturated fats, refined sugar, and highly processed foods but is
high in soluble fibre, fresh fruits, vegetables, and fish plus supplementation with omega-3 fatty
acids, omega-6 fatty acids, lecithin, and lipotropic agents such as methionine, choline, and inositol,
cysteine, vitamin C, chromium, and zinc.
(5).Atherosclerotic (heterogenous) plaque
This is the most serious indication of atheroscleromas or hardening of the arteries (147, 153). Plaque
appears as a non-translucent crystalline structure which may be as large as several large white blood
cells. Plaque formation is an indication of excess saturated fats in the diet, poor liver function, excess
smoking, and oxidised LDL cholesterol. These are most obvious under phase contrast but not so
visible under dark field.
Treatment is as for protoplasts, above.
ii. Crystals:
Note: All crystal observations below are mostly pertinent to phase contrast microscopy. Under
dark field many of these crystals appear as brightly fluorescent bodies of indistinguishable shape
and colour!
(1).Cholesterol crystals excessive
Cholesterol crystals appear as fine, elongated, shards of broken glass. They are almost colourless
and are commonly found in the blood. Unless observed in large amounts, the presence of these
crystals in the blood is of little significance in terms of nutritional status. Excess cholesterol crystals
in the blood, however, is a warning that there may be early stage plaque formation or gallstone
formation and steps should be taken to reduce cholesterol levels by cutting saturated fats and refined
sugar out of the diet. Cholesterol is biosynthesised normally by the liver and is an important
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precursor of a range of biochemically important substances in the body including bile salts and
steroid hormones (adrenal and gonadal). It is also a constituent of all cell membranes, playing a
very important role in the regulation of transport of minerals and solutes across the membrane.
Cholesterol crystals in the blood have been associated with atherosclerotic vascular disease (112).
Treatment is to put the patient on a sugar-free, fat-free, caffeine-free, chemical additive-free diet
which is high in soluble fibre and to supplement with a liver formula.
(2).Uric acid crystals excessive
Uric acid crystals appear as flat, square, yellowish coloured crystals and are normally present in
small amounts in the blood. They are bi-products from nitrogen waste generated from digestion of
protein-rich foods such as meats, fish, eggs, beans, milk, cheese, yoghurt, etc. and their production
is increased by a number of dietary factors such as sugar and sugar-containing foods, refined flour
products, alcohol, protein-rich foods (above), other acid-forming foods in the diet, and by
dehydration. Excess uric acid in the blood is indicative of degenerative conditions such as gout and
arthritis, poor kidney function, excess intake of refined sugar or caffeine, under exercise, or an acid
blood profile. Excess uric acid crystals in the blood correlates with gout (59), increases in certain
serum proteins (104), arthritis or high protein diet (129) and uremia (160). Sometimes these crystals
appear quite yellow to light brown in colour due to adsorption of ferric ions (62).
Treatment is to increase the amount of alkaline-forming foods in the diet, decrease the acid-forming
foods in the diet (particularly high protein foods), increase water intake to at least 2 litres per day,
and to supplement with lecithin and vitamin C to stimulate kidney function.
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(3).Red Pseudocrystals
The presence of red pseudocrystals in the blood is due to malabsorption in the gut (leaky gut
syndrome). These are not true crystals so are better described as pseudocrystals. The red - orange
colouration is believed to come from an antibiotic produced by the gut flora called actinomycin.
Dysbiosis, bowel dysfunction, food allergies, and poor circulation are all contributing factors in the
production of red psuedocrystals. These pseudocrystals are often accompanied in live blood with
the presence of platelets surrounded by mucopolysaccharide which indicates possible endotoxins in
the gut and/or dysbiosis.
Treatment is to put the patient on a fibre-rich diet with lots of fresh fruits and vegetables and to
supplement with acidophilus/bifidus cultures (probiotics), prebiotics, guar gums, pectin, vitamin C,
zinc, and a liver formula. Soluble fibres such as psyllium husks, oat bran, barley bran, and rice bran
are highly recommended due to their ability to promote the production of beneficial fatty acids in
the gut and not lead to aggrevation of the gut wall as is the case with hard, insoluble fibres from
wheat and corn. If food allergies are indicated, testing to establish what the allergies are and
subsequent avoidance of these foods is highly recommended for a few months followed up by re-
introduction of these foods in very small amounts one at a time to overcome the allergic reaction.
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(4).Orange Pseudocrystals
Orange psuedocrystals are another indicator of gut malabsorption/dysbiosis (see red pseudocrystals,
above).
(5).Blue Pseudocrystals
a. Dark blue crystals:
87
b. Corn Flower Blue crystals:
Dark blue pseudocrystals (a) are often found in the blood of patients who have had exposure to
pesticides and suffer from chronic fatigue. Enderlein believed that the paler blue green (corn flower
blue, b) crystals were associated with poor thyroid function which would also offer an explanation
for the fatigue aspect.
iii. Microbial Observations
(1).L-forms
88
These are bacterial variants so named because of the Lister Institute where they were described and
documented by Dr. Emmy Klieneberger-Nobel in the 1940’s (83). They are also known as
pleomorphic organisms or cell-wall deficient organisms. They appear as hazy dots or a dullish, fine
grey mist of dust-like particles and may develop into many pleomorphic forms if activated (dots,
rods, coccal forms,threads, etc) . They are quite visible by both phase contrast and dark field
microscopy. L-forms are present during bacterial infections, candida infections, or suppressed
immune activity.
Enderlein called what appear as a large accumulation of the smallest forms of L-Forms a protit veil.
If activated they can appear in many shapes and sizes as they are pleomorphic. Under certain
conditions L-Forms they may revert back to the original bacterial form.
Treatment is as described above for immune system support or to treat candida (see below) -
whichever is appropriate.
(2). Mycoplasmas
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These mycoplasmas are seen in the blood plasma. They appear as round bright structures with a
black centre. Here they are ‘donut’ shaped. They may also assume many and varied other shapes
and sizes. Mycoplasmas may also appear inside red blood cells.
These are very small free-living organisms which have no cell wall. ie. they are cell wall free
bacteria. As such they can assume a variety of shapes. They appear as motile, spherical to oval
shaped, organisms which are commonly found in the blood during arthritis, pneumonia, genito-
urinary tract infections, and neurological disease. Under dark field microscopy they usually appear
as bright (white) objects with a black dot in the centre while under phase contrast they are visible
as black motile objects about 4 - 5 times the size of chylomicrons. They can assume almost any
shape and, consequently, were probably mistaken as different microorganisms (rather than different
shapes of the same microorganism) by earlier biologists. Dr. Thomas McPherson Brown proposed
several years ago that rheumatoid arthritis was caused by mycoplasmas. He carried out years of
research at the George Washington University in USA and claimed complete remission or, at least,
major improvement from rheumatoid arthritis in the majority of his patients within 6 months of
treatment with tetracyclin drugs. The work was scorned and ignored by orthodox medicine at the
time even though they prescribe gold injections as a course of treatment knowing that gold
injections are effective in destroying mycoplasmas but the role of mycoplasmas in rheumatoid
arthritis is now being re-investigated for validity. Drs. Garth and Nancy Nicholson have also
recently published compelling data linking mycoplasma infections to Gulf War Syndrome. Using
Polymerase Chain Reaction (PCR) they were able to specifically identify mycoplasmas isolated
from the nuclei of white blood cells taken from sufferers of this debilitating disease (116) and by
treatment involving the long term (2 years) use of tetracyclines they were able to achieve some
decline in the symptoms of the disease.
Treatment is by way of boosting immune activity, as above. For patients undergoing tetracyclin (or
any other antibiotic treatment) it is important to supplement their diet with acidophilus/bifido
bacteria to help avoid possible candida overgrowth of the intestinal tract and to use the Sanukehl
preparations in conjunction with Sanum protocols to eliminate the mycoplasmas and other cell wall
deficient cells in order to restore health to the individual.
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(3). Bacterial Forms
(a). Coccal Forms
(b). Rod Forms
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These are toxic forms of infecting organisms appearing as motile rods which may have club-like
ends (dumbbell shape = macrochondrits). They may contain developing spores and can sometimes
project filaments making them the most toxic and motile forms of the organism.
Treatment is to boost and support the immune system both through diet and supplementation, as
above.
(c). Spirochaetes
Spirochaetes are possibly Leptospires [see above, section VI 3 c].
Treatment would be to restore alkaline pH (7.35) by dietary and alkalizing measures and boost
immune activity. Sanum products such as the penicillium formulas in conjunction with Sanum
therapy are also recommended.
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(4) Yeast buds
Candida yeasts buds and fungal mycelia forms are often seen whenever the gastrointestinal tract is
overgrown with that organism. Yeast forms are not such a severe sign but the fungal, mycelial forms
are highly toxic. Other ‘fungal’ forms (below) are also highly pathogenic.
Yeast (candida) buds are not easily observed under dark field but you may see a very fine outline
of the candida buds. They are, however, seen clearly as white objects about the same size as, or
bigger than, platelets when observed under phase contrast. They are indicative of an overgrowth of
candida in the gut and/or systemic candida infections of the mouth, vagina, anus, etc. Candida is
also one of the causative organisms in tinea. Antibiotics, contraceptive hormones, and hormone
replacement therapy can all lead to candida problems.
Phase Contrast:
Treatment is to remove all sugar from the diet and to supplement with acidophilus/bifidus cultures
plus a liver formula to assist detoxification. Oxygen therapies are also effective in treating candida.
If the candida problem is on the skin it can be treated topically using various agents such as iodine,
tea tree oil, methylated spirits, or douches containing acidophilus/bifido bacteria plus lemon juice.
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(5).Mycelial ‘Fungal’ forms
These can be due to pseudohyphal forms of Candida, Mucor racemosus, or other fungal agents and
are the most toxic form of the infecting agent or they may be advanced forms of development of
mycoplasmas or what Enderlein described as synacits. Immune suppression is also most likely to
accompany the presence of these organisms in the blood.
Treatment is as above for candida buds but should also include supplements to boost the immune
system, as above. These are indicators of an acid profile so increasing pH to normal is essential.
(6) Black Fungus
Black fungus is seen as thick-walled objects similar to candida in size and shape but usually have
some mycelial forms attached. It was named ‘black’ fungus by Bradford because it shows up as a
black hyphae under phase contrast unlike candida fungal hyphal forms which show up as white
structures. These are highly toxic forms of fungus and must be treated with an anti-fungal
programme immediately.
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(7) Aspergillus Drepanids
Aspergillus is associated largely with chronic infections of the bronchi and lungs but is also
associated with fungal otomycosis, and many bacterial infections. Mucor, Penicillium, and
Rhizopus may also be involved with these problems in some cases. Enderlein argued that
Aspergillus niger van Tieghem was the species present in blood and that it’s bacterial form is Koch’s
bacillus. He associated the presence of these microorganisms in the blood with health problems
such as diabetes, rheumatoid arthritis, tuberculosis, and breast cancers.
Often it is possible to observe these drepanids actually developing on the blood slide while you are
watching. Below is a series of slides showing this phenomenon over a period of around 15 minutes.
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Treatment is to use an alkalizing diet to return body pH to around 7.4 and to boost the immune
system using colostrum, vitamin C, zinc, garlic, Echinacea, etc. The Sanum treatment is to use
Nigersan plus Mucokhel as Mucor racemosus often accompanies Aspergillus related infections.
(8) Aspergillus symplast
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(9). Mucor symplast
Symplasts, and drepanids are described by Enderlein as having their origin in the process of
systatogeny which is, effectively, a coming together of protein colloids to produce dried protein
forms. Sclerosymplasts (pseudocrystals), pteroharps and derosynascites are also included in this
category of dried protein forms. The Aspergillus symplasts are typically dark in colour while those
of Mucor are white. Aspergillus drepanids have the typical ‘fish bone’ appearance and are often
seen actually growing in the blood while you observe them under the microscope.
XI. PLEOMORPHIC MICROORGANISMS

As mentioned earlier, over the last 2 centuries several investigators have identified microorganisms
in the blood that they argue can change from one microorganism to another (pleomorphic)
depending upon the state of the milieu, or terrain, of the individual but each investigator has come
up with their own set of names for the various microorganisms and their own theory as to how these
microorganisms change in shape and colour. Although Béchamp was the first researcher to come
up with the pleomorphic theory, I have chosen to outline the nomenclature of Enderlein and
Naessens who extended the work of Béchamp in more recent times. On his death bed Pasteur was
reported to have said “The microbe is nothing - the milieu is everything” – a direct admission that
Pasteur believed that Béchamp’s work was of greater significance than he was prepared to recognize
during their life time of, at times, parallel research efforts.
The Germ Theory became a medical paradigm and it proposes that all disease is caused by infection
of our normally ‘sterile’ bodies by pathogenic microorganisms from the environment. Each
different microorganism causes a different disease. It is based on the principle of monomorphism
(that each microorganism has only one form and is immutable). Despite its many inconsistencies
this theory is still held strongly by the medical system. We all know that our bodies are not sterile
but contain a number of microorganisms both internally and on our skin that do not cause us to
contract any diseases unless they undergo a major shift in balance which can be largely due to
changes in the milieu. We know that many of our gut bacteria are ‘good’ guys – beneficial to our
well being. We also know that the blood is not sterile but may contain bacteria and yeast buds -
even in healthy individuals. We also know that viruses can change from one form to another simply
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by swapping their protein coats. Unfortunately, even though there were some excellent observations
made by Béchamp, one problem he had was that he was unaware of the existence of viruses and the
nuclear material DNA and RNA that codes for each and every individual and allows for species
specificity. Enderlein identified a number of forms in the blood that are clearly not different
microorganisms (that have developed from one another) but rather, different forms of the same
microorganism. Some of the forms he identified are possibly mycoplasmas (sporoid symplasts),
candida yeast buds (thecits), CWD forms of bacteria and yeasts (basits, ascits), and chylomicrons
(symprotits). You have only to observe the blood of a person within an hour of them eating any
fatty or oily foods to see a plethora of chylomicrons. Brownian movement was well known by
Béchamp so any moving object in the blood was differentiated from inanimate objects when
describing a living particle. Microscopes at that time were limited by dark field observation only
and would not have been as powerful as the modern light microscope. Furthermore, many objects
(including some microorganisms) are, in fact, what is called dark bodies and are invisible under
dark field microscopy. These same dark bodies are clearly observed by phase contrast microscopy.
It is also worth mentioning that Enderlein published some 500 articles and pamphlets but not once
did he publish in a peer reviewed scientific journal or produce one photograph, even though that
technology was available to him. He only produced drawings of the many forms he observed in the
blood. These factors have incurred the wrath of many detractors of his work.
1. Enderlein’s endobiont theory:
a. Enderlein’s pleomorphic bodies in the blood.
Enderlein named the smallest living unit the protit and variant microorganisms formed by
pleomorphism colloids, endobiont, filum, chondrits, cystits, dimychits, spermits, symprotits,
syndimychits, and zoits, to name a few. The colloid, filum, and protit are invisible to the naked eye
under dark field light microscopy so will not be mentioned here. Some of the forms visible in the
dark field light microscope include:
(i) Symprotit
Appear as large chylomicrons moving around in the plasma, but Enderlein believed
them to actually be a primitive granulation about 1µ in diameter and a 2-, or 3-
dimensional formation from protits. Symprotits can increase in size to macrosymprotits
(approx. 2-4 µ in diameter) and are often indicative of acute infection. Other bodies
similar in shape and size may possibly be mycoplasmas, L-Forms of bacteria, or globin
proteins.
(ii) Chondrit
The chondrit is a dumbbell-shaped formation consisting of two symprotits and one
filum. It is characterized by the permanent change between filum and symprotit. These
sometimes appear as rods with round structures at each end and are possibly rod form
bacteria. They may appear as free structures in the plasma or as growths in, or on, red
blood cells and white blood cells. Small (micro-) chondrits are apathogenic and serve a
protective roleregarding our health whereas macro-chondrits, along with sporoid
symprotits) are pathogenic and associated with many diseases including arthrosis,
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epilepsy, apoplexy, neuritis, sheumatism, arrhythmias, cancer, and in the most extreme
cases, myloid leukaemia and pernicious anaemia.
(iii) Spermit
Consists of a mychit head and a filum flagella. According to Enderlein, these forms
sexually copulate with bacteria and, as a result, degrade them into apathogenic primitive
forms. Sometimes spermits appear in the plasma along with symprotits and are
associated with virulent/acute infections. They are barely visible as very small bright
flashes moving around in the plasma and sometimes not even seen under dark field.
They act as bacteriophages with specificity for bacterial forms of Mucor racemosus.
(iv) Fibrin (thick filit formation)

Fibrin net indicative of ‘Mucor burden’ usually accompanied by erythrocyte rouleax or
aggregation and is indicative of ‘viscous’ blood, liver stress, and intestinal stress.
Enderlien described fibrin as a thick filit formation rather than a protein formed from
fibrinogen in the liver.
(v) Mychit
The primary nucleus which develops as the symprotit accumulates proteins and lipoid
material around it and the whole structure grows to about 5µ in diameter. This is the
primary bacterial form according to Enderlein. The distinct nucleus is the mych which
usually resides close to the mychit membrane, the accumulated protein becomes the cell
plasma and the outside is lipoid material which becomes the cell membrane.
(vi) Cystit
An enlarged mychit form.
(vii) Thecit
This is a form in which the enlarged nucleus of the cystit has divided into many small
‘nuclei’.
(viii) Sporoid symprotits

These appear as small donuts and were described by Enderlein as due to the upward
development of the symprotits into pathogenic forms. He implicated them in situations
of liver toxicity and toxic burden. These bodies are most probably mycoplasmas and
under dark field appear as bright circles around 1 - 2µ in diameter. In phase contrast
they are dark circles with a white centre – appearing like very small red blood cells.
(ix) Macrosymprotits
Enlarged symprotits in the plasma may be indicative of acute infection and/or fever.
These may also be mycoplasmas.
(x) Colloid thecits

These are thecits with moving flagella around their entire surface and filled with
‘invisible’ colloid (protein) material. They are around 6 - 8µ in diameter. Enderlein
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believed them to be an ambivalent form of the endobiont. These structures appear as

similar to echinocytes except the flagella move very rapidly on the surface of colloid
thecits propelling them along through the blood plasma.
(xi) Dioecothecits
These are similar in size to colloid thecits, have flagella around their surface and are
filled with endobiont (microchondrits and spermits). Although ambivalent forms, they
act as stores of spermits so they are at the ready to defend us whenever there is upward
development of the endobiont to pathogenic forms.
(xii) Ascits or Bacterial rods (eg. Leptotrichia buccalis)

Appear as rod forms about 3 -10µ long. These forms are often moving in the plasma
and are associated with infections, allergies, sinusitis, etc. They appear as bacterial rod
forms.
(xiii) Thrombocytes (platelets)

Enderlein described thrombocytes as having a number of nuclei (3 – 7) and projections
of filum from their outer surface. He claimed that thrombocytes were of plant origin and
were related to the endobiont. We now know that they are produced in the bone marrow
from specific blast cells (the megakaryoblasts) and are essential for good health and
well-being.
(xiv) Mucor Symplast

These large bodies are often associated with arthritic/rheumatic problems. These bodies
appear as protoplasts which are always very pale to white in colour.
(xv) Aspergillus Symplast

These very large dark bodies are a conglomeration of parasitic forms of Aspergillus
niger and are seen in the plasma of individuals with major physiological disturbances
particularly those involving calcium metabolism (bones), connective tissues, lungs,
bowel, lymph glands and lymphatic system or mucous membranes.
(xvi) Mixed Symplast

These very large bodies are probably what we describe as Atherosclerotic Plaque. They
are associated with congestion of the blood and may also appear in severe pathological
situations such as cancers.
(xvii) Dark Sclerosymplast

These large bodies are often associated with kidney stress, heavy infections, and may
be seen in the plasma of individuals with cancer.
(xviii) Sclerosymplast
These large bodies are associated with abdominal problems/malabsorption from the gut.
(xix) Yellow Symplast
These bodies may indicate pancreas or small intestine problems.
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(xx) White Symplast

These bodies may be indications of kidney stress.
(xxi) Disc-Shaped Segmented Symplast

These are often associated with urogenital tract infections/acute cystitis.
(xxii) Red/Orange Pseudocrystals (Symplastss)

These are most often associated with abdominal problems (eg pancreatitis, cholecystitis,
dysbiosis – gut malabsorption).
(xxiii) White Crystals

These are probably uric acid crystals and are associated with kidney stress, arthritis, and
rheumatic problems. They are plate-like structures and under phase contrast appear as
yellow crystals.
(xxiv) Reticulocytes
These are what Enderlein describes as parasitized erythrocytes filled with chondrit-
dendroits and are most probably reticulocytes (nucleated erythrocytes) or blast cells
indicative of bone marrow hyperplasia. Enderlein argues that they are a sign of heavy
metal toxicity.
.
(xxv) Leucocytic Plasma Invasion
The ‘invasion’ of white blood cells is sometimes seen in as granules in the cytopolasm
of T- and B-Cells during viral infections. Large bodies in the cytoplasm of granular
leucocytes mostly indicates that they are eosinophils or basophils which were not
described by Enderlein. L-Forms and mycoplasmas are known to inhabit the
cytoplasm of white blood cells.
b. Bacteriophages and Spermits.

Bacteriophages are perhaps the most widely spread and diverse microorganisms in the
biosphere, are ubiquitous in Nature, and can be found in all reservoirs populated by
bacterial hosts such as sea water, the soil, and the intestines of animals. They have been
used as antibacterial agents in the former Soviet Union and Eastern Europe for over 60
years as an alternative to antibiotics and are seen as a possible therapy against multi
drug resistant strains of many bacteria (Wikipedia). In ancient times it was believed
that certain river waters had the ability to cure some infectious diseases. In 1915,
British biologist Frederick Twort, discovered the small agents that infected and killed
bacteria. He believed them to be either a stage in the life cycle of the bacterium, an
enzyme produced by the bacteria themselves, or a virus that grew on and destroyed the
bacteria. In 1917, Félix d’Hérelle (34) proved the agents to be a “bacteria eating” virus
which he called a bacteriophage and showed that dysentery could be cured using
bacteriophages derived from the dysentery bacillus. Bacteriophages replicate by
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injecting their nuclear contents (RNA or DNA) into the bacterium and then use the
bacterial DNA to manufacture multiple copies of themselves. This action of
bacteriophages is identical to the sexual union between spermits and higher forms of
the endobiont (bacteria) described by Enderlein. Both the actions of bacteriophages and
spermits are species specific and result in the destruction of bacteria and offer a way in
which the health of the host can be restored. Enderlein was very aware of
bacteriophages and their identical nature to his spermits. He described the action of
spermits in the following way: “…….bacteriophages ranging in size from 0.1µ down to
0.01µ and even smaller. These flagellated and lively forms, ie. a granule (symprotit)
with a bare filum bearing no terminal granule, forms in bacterial colonies from the
germination of the bacterial nuclei (mych) – ie. from flagellum components. Next they
copulate with other mych, leaving the bacterial cell in the process, shrinking
considerably in size due to the multiplication by fission which always sets in after
copulation – and can, if the pH is right, cause all mych to migrate out of the bacteria
and swarm about as so-called bacteriophages, in order to begin the cyclogenic ascent
all over again.” (43). There is an acceptance by modern day medicine that
bacteriophages exist and have a species specific antibacterial effect but they adhere to
the view that bacteriopahges are not part of a life cycle of that specific bacterium, rather
some sort of an invading outsider. Enderlein, however, was quite specific in describing
bacteriophages (spermits) as an integral part of the bacteria’s life cycle, driving it back
from a pathogenic form to an apathogenic form as part of the defensive mechanism of
the body. Once the bacterium has been rendered avirulent by the bacteriophage/spermit
it is excreted from the body via the normal excretory organs (epithelium, ureters, lungs,
bronchi, and intestinal tract). The result of these bacteriophage/spermit sexual
interactions with bacteria is that the higher forms (bacteria) present in the milieu are
reverted back to lower forms (spermits and microchondrits) thus restoring the
individual to a state of health and the upward development of the life cycle (cyclode) of
that bacterium can only start again if the condition of the milieu changes to favour that
process – primarily through a shift to lower pH.
There are a few more forms described by Enderlein which are included in the book “Introduction
into darkfield diagnostics - The examination of the native blood according to Prof. Dr. Gunther
Enderlein” by Cornelia Schwerdtle and Franz Arnoul publ. Semmelweis-Verlag (1993) ISBN 3-
925524-02-9 along with colour plates and sketches. As mentioned above, several of the forms
described by Enderlein have been identified as identifiable microorganisms, chylomicrons, uric acid
crystals, and other things since the advent of phase contrast and differential interference light
microscopy.
What is the endobiont? According to Enderlein it is the primary symbiont of plant origin that
culminates into the fungus Mucor racemosus Fresen, the bacterial form of which is the Leptotrichia
buccalis. He argues that the endobiont is of a fibrin nature and devours animal proteins. He also
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states that it is present in all living tissues and healthy blood and it is only when it develops into
higher forms that it becomes pathogenic. Bradford (18) described endobiont as candida albicans
while Gerner (58) isolated it from blood and identified it as aggregations of hemichrom from the
breakdown of haemoglobin of old and damaged red blood cells. The hemichrom was mainly
composed of the protein globin and was not a living microorganism and was not of plant origin!
The reason Gerner and Bradford came to different conclusions is probably because Gerner isolated
small vibrating bodies from the blood plasma (symprotits) while Bradford compared yeast (colloid
thecits) and ‘fungal’ (ascits, synacits) structures that he observed under phase contrast with that seen
under dark field.
Despite all of the above, there are a few things that are note-worthy from Enderlein’s work:
c. There are a number of different microorganisms that can be observed in the blood, some of
which (the L-Forms, mycoplasmas and candida) can undergo pleomorphism.
d. There are long thread-like microorganisms (L-Forms), rod forms (Leptotrichea), spherical
forms that take on a range of shapes (L-Forms and mycoplasmas), dumbell forms (rod form
bacteria), bud forms (candida), ‘fungal’ forms (Aspergillus, candida, or Mucor racemosus),
and fibrin forms (filum dedroids, fibrin, and lipid ribbons).
While examining the blood of patients you will encounter some of the forms described by Enderlein
and, if you have time, you may well observe them growing or even changing shape. Those forms
that are not the ‘usual’ bacterial rod forms or coccal forms, yeast buds, yeast pseudohyphae forms,
or fungal mycelia forms may well be intermediate forms of some of these microorganisms but,
whatever the case, it is well worth recording your observations for later appraisal of the patient’s
condition. Keep in mind that the blood is not sterile and that bacterial and fungal spores are
constantly in the environment and would be present in the air and on the slides we use for live blood
preparation. Also remember that the blood is the perfect medium for growing microorganisms.
Michael Coyle (Nu-Life Sciences) has drawn up a life cycle of polymorphic microorganisms
observed in the blood as described by Enderlein (Sketch courtesy of Michael Coyle):
:
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Many of the microorganisms described by Enderlien have been observed, mainly as Mycoplasmas
and L-Forms of bacteria, in the blood of patients both healthy and in ill health (104, 115).
Sketches and a list of most of these forms and their meaning according to Enderlein is presented in
the following two diagrams prepared by Dr. Beilin:
104
105
In addition to Enderlein’s observations on microorganisms in the blood he made some observations

on the blood cells. Even though some of his observations are somewhat consistent with our most
up to date information he was quite incorrect on many others. For example, rouleau formation of
red blood cells he suggested was due to endobiosis with congestion of blood supply and curved
rouleau formation due to intestine stress (according to Prigge). From what we now know, Prigge
was correct and rouleau is due largely to poor digestion – particularly of proteins and fats. Protein
linkage he assigned to liver stress when it is actually due to an alkaline profile or low stomach
acidity. Anisocytois he correctly assigned to anaemia. Poikilocytosis he assigned to a number of
things including endobiontic burden and infestation of erythrocytes. Target cells are a result of
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anaemia but he related them to slight pathogenicity, echinocytes are due to oxidative stress but he
designated that they were due to a high degree of endobiosis, and so on. Remember, Béchamp,
Pasteur, Enderlein, Bernard, and other early biologists did not have the advantage of today’s
technology (scanning electron microscope, X-ray diffraction, high pressure liquid chromatography,
etc.) but they did their best with what they had available. For this reason it would seem that
following the now out-dated ideas of Enderlein 100% would be to ignore both up to date research
and that which has stood the test of time. We should accept the parts he got right and reject those
he did not. For further reading on Enderlein’s work I would recommend the book “Unappreciated
Friend or Unsuspected Foe” by Dr. Maria-M. Bleker (14) and his “Bacteria Cyclogeny” (see
p.142) .
2. Naessen’s Somatide Cycle:
Naessens described how it was possible to see what he called somatides, spores, and double spores
in the blood of healthy individuals. He isolated the somatids from blood and put it into culture then
observed (through his Somatoscope) the somatids undergo a polymorphic cycle (the Somatide
Cycle) in which were produced bacterial forms, rod-like forms, granulated bacterial forms, yeast
forms, ascospore forms, mycelial forms and a thallus form that burst to release somatides and the
cycle was then repeated. In the course of this cycle a substance he named the trephone was
produced. The trephone is a ‘proliferative’ hormone indispensable to cellular division. Without it,
he says, life does not exist! In healthy individuals the cycle stops at the double spore stage due the
presence of trephone inhibitors in the blood. These are substances like copper, mercury, lead, or
organic substances such as cyanhydric acid.
He concluded the following:

a. Cellular division requires the presence of the somatide (which is in either the animal
or the plant domain).
b. Trephones are elaborated by the somatide.
c. The somatide is capable of polymorphism. This polymorphism is controlled by
inhibitors in the blood.
d. A deficiency in sanguine inhibitors permits the elaboration of large quantities of
trephones which, in turn, lead to disorders in cellular metabolism.
e. The degenerative diseases are a consequence of these disorders.
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A diagram of the Somatide Cycle follows:
Note: The best one can do when observing the blood is to note anything unusual and keep an open
mind as to what that observation may mean in relation to an individual’s health status. If you see a
specific form showing up in the blood of everyone who has a particular health problem then you
may be able to use it as a marker for that specific malady. To date, after working on the blood from
over 12,000 patients I have not been able to establish any specific new markers but you may be
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more fortunate. Generally, keep in mind that any specific observation you make may be indicative
of a range of health problems so keep quizzing the patient to find out what their problem may be.
XII. MICROBES IN PERIPHERAL BLOOD – A MODERN

PERSPECTIVE:
Firstly, it is important that you know what the various bacterial forms look like and how you
can distinguish between them based on their size and shape.
1.Shapes of Microorganisms:
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2.Relative Size of Microorganisms in Blood:
110
3. L-Forms of Bacteria:
L-Forms of bacteria are basically cell wall damaged and cell wall deficient bacterial (CWD)
forms. Under certain conditions they may revert back to the bacterial form. L-Forms may be
apathogenic or pathogenic and are highly pleomorphic ranging in size from 0.1µ in size up to
as large as 70µ. They can also take on a huge variety of shapes from discs and spheres to odd
‘hyphal’ type shapes to thin filaments as long as 60 - 70µ.
In 1895 Richard Pfeiffer first described an “altered form” of the bacterium Vibrio cholera
which was most probably the first report of an L-form bacterium. He noted that this altered
form was very difficult to observe under dark field microscopy.
During the 1890’s Ernest Alquist, a friend of Louis Pasteur, cultured an altered form of
bacteria and found that it’s requirements for growth differed quite markedly from that of
‘normal’ bacteria.
In the 1940’s a German scientist, Dr. Emmy Klieneberger-Nobel, extensively studied these
altered forms of bacteria at the Lister Institute in Britain and named them L-Forms (after the
institute) and perfected a method of growing them on blood serum agar. She worked mainly
with L-Forms of Streptobacillus moniliforme but also mycoplasmas.
Also during the 1940’s and into the 1950’s Dr. Louis Dienes was able to produce several L-
Forms of bacteria (in particular Salmonella typhosacoule) by treating the bacteria with
penicillin, other antibiotics related to penicillin, chemicals, high levels of amino acids, lithium,
calcium, chromatin, and mercuric salts while undertaking research at Harvard Medical School.
Dr. Virginia Wuerthele-Caspe Livingston extended the work of Dr. Dienes by culturing L-
Forms from patients with scleroderma, noting that they could vary in size from as small as
viruses to that of bacteria up to that of fungal and yeast spores. She was also able to culture and
grow L-Forms from various human cancerous tumours.
In 1975 Dr. H.M. Butler and his team wrote a review of L-Forms describing their resistance to
penicillin and their ability to change form. The group concluded that L-Forms may be
clinically significant in cases of chronic and recurrent infection. Also during the 1970’s Drs.
Bisset and Bartlett identified L-Forms of Bacillus licheniformia during the different stages of
its life cycle and argued that the L-Form variants of bacteria may well have been previously
incorrectly classified as other species of pathogens.
During the 1980’s Dr. Emil Wirostko, at Colombia University, cultured and photographed L-
Forms that he was able to isolate from white blood cells he extracted from the fluid inside the
eyes of patients who suffered from sarcoidosis, juvenile rheumatoid arthritis, and Crohn’s
disease while observing these L-Forms under the electron microscope. He noted that the L-
Forms were encased in a protein membrane or exoskeleton that protected them from being
digested by the white blood cells (lymphocytes, monocytes, and polymorphonuclear
leucocytes) that they resided in.
Dr. Alan Cantwell discovered a stain for L-Forms and was able to identify L-Forms of
Stroptococcus B from lymph nodes and blood of patients with HIV as well as lymph nodes and
skin of patients with the lung disease sarcoidosis. He noted that the L-Forms could grow into
very large forms that are now known as Russell bodies. When examining tissue samples from
skin, lymph nodes and other organs from patients who had died of Hodgkin’s lymphoma and
other cancers he found copious amounts of L-Forms including round forms resembling
staphylococci species, rod forms resembling corynebacteria.
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Dr. Lida Mattman, a senior bacteriologist at Massachusetts University also extensively studied
L-Forms using fluorescent antibodies and staining techniques to view them with a light
microscope. She identified two different species of L-Form bacteria in patients with
Parkinson’s disease, the L-Forms of Borrellia burgdoferi in patients with Lyme disease and
that of Chlamidia pneumonia in the blood of patients who had suffered a pulmonary
thrombosis. She also found L-Form bacteria resembling that of Mycobacterium tuberculosis in
the blood of patients with sarcoidosis.
Many L-Forms exist within the red and white blood cells. Parasitism of red blood cells by L-
Forms occurs to a minimal degree in every person and, according to Mattman, represents the
escape of bacteria from heavily populated regions in the body such as intestines, skin, oral
cavity, and lymph nodes into regions of the body usually considered sterile. In septicaemia and
some chronic infections the pathogens can best be found in the white blood cells.
CWD forms of Bacillus licheniformus resides in erythrocytes of up to 30% of healthy
individuals.
CWD forms of Staphylococci commonly reside in erythrocytes of healthy individuals as well
as in patients with pulmonary tuberculosis.
Sarcoidosis patients exhibit intraerythrocytic CWD forms of Mycobacterium.
Karposi syndrome patients exhibit intraerythrocytic CWD forms of fungi plus fungal forms in
the plasma and involved tissues.
Isopathic hemaruria involves CWD forms that revert to Streptococcal-type bacteria.
Nephrotic syndrome patients exhibit CWD forms that revert to Staphylococcal-type bacteria.
During gonorrhea infections CWD forms of Neisseria gonorrhea persist in the neutrophils.
CWD forms of Borrelia burgdorferi are present in white blood cells of patients with Lyme
disease.
CWD forms of Salmonella typhi (typhoid bacillus) grow well inside monocytes in the lymph
tissues of Peyer’s patches.
Variant forms of CWD bacteria may act as haptens and stimulate production of hemolytic
antibodies. eg. In syphilis patients the CWD form of Treponema pallidum lives
intraerythrocytically as a tiny unit, stimulating the host to regard the red blood cell treponeme
conjugate as foreign material.
In 1997 Dr. Gerald Domingue and his team at Talane University published an extensive review
of chronic bacterial infection in which they claimed that L-Forms of bacteria have the ability to
lie dormant in the host until conditions favour them entering blood and tissues where they can
become pathogenic.
L-Form bacteria (also known as stealth bacteria) have been shown to be associated with several
diseases in man. They include:
- Tuberculosis
- Scleroderma
- Various cancers
- Sarcoidosis
- Rheumatoid arthritis
- Chronic fatigue syndrome
- Lyme disease
112
- Parkinson’s disease
- Kawasaki disease
- Pulmonary thrombosis
- Multiple sclerosis
- Inflammatory bowel disease
- Lupus erythematosus
- Diabetes mellitus
- Wegener’s granulomatosis
In Adelaide, South Australia, Trevor Marshall, a biomedical engineer, contracted the disease
sarcoidosis which has no medical treatment other than the use of corticosteroids to bring about
partial and temporary relief of symptoms. He read the work of Wirostko and Nilsson who had
both related sarcoidosis to being caused by L-Forms of the bacteria Rickettsia Helvetica and
also noted that his personal symptoms were exacerbated by exposure to sunlight. Marshall
carried out decades of research on L-Forms and was able to determine how L-Forms were able
to dysregulate the immune system and persist in the body. From his model he was able to
develop a protocol that uses pulsed, low dose antibiotics, an angiotensin II receptor antagonist
(losartan) to stimulate the immune system and eliminated vitamin D from the diet (and
exposure to sunlight) to kill off L-Forms in the body. The Marshall protocol has been used to
successfully treat a wide array of chronic diseases including chronic fatigue syndrome,
fibromyalgia, sarcoidosis, lupus, chronic Lyme disease and rheumatoid arthritis but it has its
detractors.
4. Mycoplasmas in peripheral blood:
Mycoplasmas are cell wall deficient microorganisms that exhibit a high degree of
pleomorphism. Although microscopically indistinguishable from L-Forms, they differ from L-
Forms of bacteria in that they are not simply bacterial species that have lost their cell wall
through antibiotic treatment, chemical damage, etc. – they are microorganisms that lack a rigid
cell wall. They are ubiquitous in nature and have a high requirement for cholesterol or related
steroids for their growth. Organic gold salts inhibit their growth.
They may exist as very small granules of 0.125 to 0.3µ in diameter which is the minimal
reproductive unit. These granules can flatten and grow to an irregular shaped mass of 0.4 –
0.9µ in diameter and, as growth continues, they may appear as larger, disc shaped (donut
shaped) bodies of 1 - 2µ diameter. The larger bodies undergo fission to produce many of the
smallest granules that then undergo a new growth cycle (78, see below). In addition to the disc
shapes, mycoplasmas can assume a variety of shapes from granules of virus sizes through disc-
like and amoeboid structures, to rings, clubs, filaments of up to 100µ in length, and vibrionic
and star-like forms.
Mycoplasmas are a commensal of the oral cavity and the genital tract in man and are associated
with various genito-urinary tract infections in women and non-gonococcal urethritis in men.
They have been shown by Garth and Nancy Nicholson to cause Gulf War syndrome (116) and
may well be involved as causative agents in chronic fatigue syndrome and rheumatoid arthritis.
Medical treatment involves long term administration of the antibiotic tetracycline.
113
5. Leptotrichia buccalis:
L. buccalis is an obligately anaerobic, gram negative rod form bacteria belonging to the
Bacteroidaceae family. It has also been, at times, indistinguishable from Fusobacterium
fusiforme (60). It appears as straight to slightly curved rod forms that are 10µ long x 0.7 -1.2µ
in diameter and are non-motile and non-spore forming. In some cases (when grown on a hard
medium) they may assume the shape of two rods banded together to form a short filament with
a slight taper at the free ends.
L. buccalis was first described in the late 1800’s by Trevisan (prior to Enderlein) and is mostly
found in the oral (buccal) cavity but may also be found in the genito-urinary tract. Until the
1980’s it was considered not to be pathogenic to man. Recent research, however, has linked L.
buccalis to a number of diseases in man including: bacteremia in patients with acute
myelogenous leukemia (12), cancer (151), and immunocompetent patients, mucisitis and
esophagitis (133), gingivitis, secondary infections subsequent to chemotherapy, endocarditis in
patients with prosthetic aortic valve (68), cavity pneumonia and scepticaemia (111). It is
associated mainly with oral infections due to breaks in the mucosal wall of the mouth, is most
prevalent in immune compromised patients (eg AIDS sufferers, patients with cancer
undergoing chemotherapy, patients on long term cortisone therapy). It is frequently
accompanied by neutropenia.
114
6. Pathogenic Fungi/Moulds:
a.Moulds
There are four main varieties of common saprophytic moulds (Rhizopus, Mucor, Aspergillus,
and Penicillium) three of which were described by Enderlein as being present in the blood
under certain conditions involving severe acidosis and which share some commonality in terms
of their cycles (cyclogenies): Mucor, Aspergillus, and Penicillium differ in their morphology
and epidemiology. Rhizopus and Mucor are phycomycetes with non-septate hyphae, asexual
sporangiospores, and sexual zygospores which are formed by two hyphae at their tips.
Aspergillus and Penicillium are either ascomycetes or fungi imperfecti, having septate hyphae,
asexual conidia and, in some cases, ascospores. Conidial chains of Aspergillus arise from
finger-like “sterigmata” which radiate without branching from the expanded bulbous tip of the
conidiophores. Those of Penicillium arise from sterigmata borne on the tips of several terminal
branches of the conidiophore.
All of the saprophytic mould species are found in infections of the lungs and bronchi in man.
Aspergillus is the main problem as it will grow on damaged bronchus and lung tissues,
particularly after a primary bacterial infection of these tissues such as bronchiectasis,
tuberculosis, or pneumonia. Exposure to the spores of any of these mould species can lead to
allergies and asthma conditions. Aspergillus niger, and sometimes Mucor, causes otomycosis
which is a sub-acute or chronic infection of the ear.
b. Yeasts
The only important pathogenic yeast species is Candida albicans which produces superficial
infections of the skin (cutaneous candidiasis) and mucous membranes (oral and vaginal
thrush). It also causes broncho-pulmonary infections, secondary intestinal infections, and
infrequently, septicaemia and deep blood-borne infections such as meningitis, endocarditis, and
pyelonephritis. Infection is usually due to weakening of immune function through bacterial or
viral infections, diabetes, leukaemia, AIDS, iron-deficiency anaemia, neo-natal debility,
senility, alcoholism, drug addiction, antibiotic therapy and cortisone therapy. Infection is
mostly endogenous (from the intestinal tract, skin, mouth, and faeces) but occasionally is
endogenous such as infection of infants from their mother or from other infants in a maternity
hospital situation.
7. Moulds and Fungi in peripheral blood:
Using PCR techniques it has been possible to test for the presence of moulds and fungi in
peripheral blood with great sensitivity and accuracy. Previous techniques involving isolation
and culturing from blood samples have been, at best, limiting. Aspergillus, Mucor, and
Penicillium moulds and Candida yeasts have all been detected in blood using these techniques,
particularly in peripheral blood from immune compromised patients with HIV, acute myeloid
leukemia, acute lymphoblastic leukemia, non-Hodgkin’s lymphoma, myelodysplastic
syndromes, severe aplastic anaemia, osteomyelofibrosis, and other cancers (138, 41,134). In
some cases the fungemia caused by these microorganisms was asymptomatic (147) so their
115
presence in the blood is not always indicative of a degenerative, potentially fatal, infection.
However, their presence is good evidence of the pleomorphic nature of these microorganisms.
8. pH, Oxygen and the growth of Microorganisms:
Microorganisms vary greatly in their requirements for growth factors, particularly concerning
nutrients, pH, and oxygen levels. Regarding oxygen, there are two main types of
microorganism; those that require oxygen for growth (aerobes) and those that grow best in an
oxygen-deficient medium (anaerobes). Aerobic bacteria such as Tubercle bacillus grow best in
aerated tissues (lungs) whereas anaerobic bacteria such as Clostridium welchii grow best in
oxygen deprived tissues like the intestines, lacerated wounds, and dead tissues.
Generally, microorganisms thrive in a nutrient rich medium that is maintained at body pH

(7.4). Most commensal and pathogenic bacteria grow best at neutral to slightly alkaline pH (7.3
– 7.4). As bacteria grow, they produce acidic waste products (acetic acid, formic acid, lactic
acid and succinic acid) that lower the pH of (acidify) the milieu. If there is a high level of
bicarbonate to buffer these changes in pH then there will be no progression from
predominantly bacterial forms to fungal forms. If, however, there is low buffering capacity in
the medium then the pH will decrease until the medium becomes acidic thus favouring the
growth of opportunistic fungi/moulds. There are some exceptions to the rule, however, and the
anaerobic bacteria Lactobacilli favour an acidic medium whereas Vibrios prefer an alkaline
medium. The tubercle bacillus is highly resistant to both high and low pH so can grow happily
in almost any medium.
9. Acid-Base Balance – The milieu:
The ability to maintain a constant composition of the extra-cellular fluid (the milieu intérieur
of Claude Bernard) is a most significant and important advancement in evolution. It allows for
the adaption of living organisms to a changing environment.
Approximately 20% of all body weight is attributable to extra-cellular fluid (the milieu) while
around 50% of total body weight is contained within the cells (intra-cellular fluid). Of the
extra-cellular fluid approximately 75% is intercellular fluid and 25% is blood plasma. Blood
plasma is the transport vehicle through which cells make contact with other cells and the
environment. Other extra cellular fluids which contribute only a very small percentage of total
body weight include cerebrospinal fluid, synovial fluid, aqueous and vitreous humors, and
lymph fluid.
The main cations present in intra-cellular fluid are potassium and magnesium while in extra-
cellular fluid it is sodium. Anions in intra-cellular fluid include phosphate, sulphate and
proteins while in extra-cellular fluid it is chloride and bicarbonate. Osmotic pressure is
regulated mainly by calcium, magnesium, phosphate, and proteins. Apart from proteins and
bicarbonate content, the electrolyte composition of blood plasma is very similar to that of sea
water. Sea water is also much higher in magnesium and sulphate ions.
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The cell membrane allows potassium ions to diffuse into the cell and exports sodium ions from
the cell via an active transport ATP-dependent sodium pump.
Blood plasma cations are mainly sodium (90%) with some potassium (5%), calcium (3%), and
magnesium (2%). The anions are mostly chloride (70%) with some bicarbonate (15%), protein
(9%), organic acids (4 – 5 %), biphosphate (1%), and sulphate (0.5%). Saline used clinically is
a 0.9% sodium chloride solution which is approximately isotonic with blood.
Most changes in electrolyte and fluid balance occur in the extra-cellular fluid and diversions
from the normal relationships may be from 4 main areas:
Osmotic pressure
Volume
Composition
pH
Osmotic pressure is regulated by the hormones vasopressin (increases water reabsorption) and
aldosterone (increases sodium reabsorption).
Volume is largely regulated by the plasma proteins (particularly albumin) which increase water
uptake, and total available sodium.
pH is regulated mainly by the buffering action of bicarbonate but haemoglobin also has some
buffering action on the blood. In extra-cellular fluid the bicarbonate buffer is produced
primarily from CO2 which is constantly being produced through cellular respiration. The
buffering action of haemoglobin is thought to be due to CO2 diffusing into the red blood cells
and reacting with haemoglobin to form bicarbonate anions which move out of the red blood
cells into the plasma, exchanging with chloride ions from the plasma.
Protiens and phosphate anions may also assist in enhancing the buffering capacity of the blood.
The kidneys control plasma concentrations of bicarbonate and carbonic acid thus playing a
significant role in maintaining extra-cellular pH.
Reduced pH of extra-cellular fluid stimulates respiration, increasing CO2 concentration and
raising pH back to normal. The reverse also applies.
Ketone bodies produced during ketosis (eg diabetes or a ketogenic diet) are powerful acidifiers
of the blood plasma thus high protein diets should be avoided if good health is to be
maintained.
Glutamine can produce ammonia which is able to alkalise the blood and reduce acidification.
Another source of buffering is sodium/potassium exchange (through ATP’ase) in cell
membranes. Sodium can exchange for H+ as well as potassium ions so this process can
contribute to changes in extra-cellular pH.
The simplest way of elevating pH is by administration of sodium bicarbonate.
Vomiting and diahorrea both lead to ketosis, dehydration, and acidosis.
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Changes in the milieu can be due to influences on pH, trace element content, vitamin and
mineral content, electromagnetic potential of cells, red-ox potential of cells, and, above all,
diet. Vegan diets are alkalizing and high protein diets are acidifying.
Enderlein argued that provided the milieu is in an ideal state it does not favour the growth of
microorganisms but rather turns them back into the ‘normal’ apathogenic forms – the protits.
Destroying bacteria by the use of drugs such as antibiotics has two main outcomes:
The development of viral problems

The development of cell wall deficient microorganisms such as L-forms which are able
to revert back to infective bacterial forms once the milieu conditions change to become
favourable to the upward development of these microorganisms.
An acidic medium favours pleomorphism and the upward development of fungi, bacteria, L-
Forms, and mycopolasmas but not all disease is due entirely to movement of the milieu to
lower pH values. At high pH (alkalosis) many disease states can also occur.
pH of the blood may vary from around 7.2 (acidosis) to 7.6 (alkalosis) during times of severe
stresses on the body, poor diet, disease states, etc., however, in a 'normal', healthy state the buffering
capacity of the blood will keep the pH maintained at an average value of 7.4. If the pH of the blood
is low (below 7.3) a state of acidosis will prevail. In this state many degenerative processes in the
body are activated such as arthritis, gout, ulcers, and other inflammatory conditions. Symptoms
associated with acidosis include frequent sighing, insomnia, water retention, recessed eyes,
rheumatoid arthritis, migraines, low blood pressure, constipation alternating with diarrhoea, burning
in the mouth and under the tongue, sensitivity of teeth to vinegar and acid fruits, bumps on the
tongue or roof of the mouth, and inflammation of tissues. Causes of acidosis are many and varied
but include liver, kidney, and adrenal disorders; improper diet; malnutrition; obesity; ketosis; anger,
stress, and fear; anorexia; toxaemia; fever; excessive intake of acidic vitamins such as vitamin C
and nicotinic acid (B3); and ingestion of acidic drugs such as aspirin. Conversely, if the pH is too
high (above 7.5), a state of alkalosis prevails and this can lead to sore muscles, creaking joints,
bursitis, bone spurs, drowsiness, fatigue, protruding eyes, hypertension, hypothermia, seizures,
oedema, allergies, night cramps, asthma, chronic indigestion, night coughs, vomiting, overly
viscous blood, menstrual problems, prostatitis, constipation, and skin thickening with burning
and/or itching. Alkalosis may also cause calcium build-up in the body. Causes of alkalosis are few
but would include excessive intake of alkaline drugs such as antacid tablets and lack of oxygen
intake due to inactivity but it can also be the result of high cholesterol, endocrine imbalance, poor
diet, diarrhoea, and osteoarthritis.
Bacteria and fungi compete for the same nutrients so fungi have a ‘trick up their sleeve’. They
produce chemicals that destroy bacteria (antibiotics) which gives them a great survival
advantage. For this reason the growth of fungi and bacteria are mutually exclusive and only
one form will grow in the same milieu at any one time. As pH is a factor in the growth of
microorganisms, it is not surprising that most bacteria will grow best at neutral to slightly
alkaline pH while fungi will grow best at low pH (below 6.8). If we change the pH of the
body’s milieu we can influence the growth of these microorganisms. By adding bicarbonate to
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allow great buffering capacity to the milieu we are able to increase the pH to a normal level
(7.4) and maintain it at that level. This will effectively halt the growth of fungal forms.
Fungal forms only exist in the blood in extreme circumstances (chronic, degenerative diseases
where the immune system is compromised) and only appear in the early mycelial stages of
growth. The blood never becomes acidic – only less alkaline – so it does not favour the growth
of fungi through to their terminal stages. The only time the conidial (terminal phase) form is
seen is after death when the blood and tissues become acidic and the fungi/moulds play a role
in the destruction and elimination of dead tissues. Enderlein also said that the only fungal form
we can see in the blood is the mycelial form (of Mucor racemosus) and that it was mostly
associated with advanced cancerous tumours. The mature Culminante (conidium bearing form
is only seen outside of the body.
Bacteria, L-Forms, motile rods, tubular strands, and Mycoplasmas, are all consistent with being
cell wall deficient forms and have been described in whole blood as E. coli and Staphylococcus
aureus (100), pleomorphic bacterial forms associated with tumors in humans and cancers in
animals (97), and associated with carcinoma, diabetes or alcohol abuse induced pyogenic abcesses
in the liver (154). In this latter study the microorganisms were identical to those from the gut flora.
In 2001, Dr. Peter Schneider published an article on Cell Wall-Deficient (CWD) forms of
bacteria and fungi (including candida) in which he addressed the upward development of these
microorganisms in blood (134). As outlined, above, modern conventional microbiologists have
been able to show that changes in growth phases of fungi and bacteria are able to take place in
the blood. These changes are pleomorphic and involve CWD forms of the microorganisms.
Using this information in conjunction with Enderlein’s dark field microscopy observations,
Schneider states that the “CWD forms of pathogenic bacteria are the most important microbial
cause of the chronic nature of illnesses in every case”. Growth of the pathogenic bacteria inside
a living organism occur, according to Schneider, mainly due to general or localized excess of
energy as a result of blockages while that of fungi and yeasts occur primarily due to general or
localized lack of energy. If this is so, it would indicate that energy production (or lack thereof)
is a major influence in the upward development of pathogenic microorganisms, primarily as
CWD’s. According to Schneider, blockages of energy to the cells and tissues through actual
movement of energy material (metabolites), vital energy, or emotions will lead to an
accumulation of energy in the blood which will drive the production of CWD bacterial forms.
Once the cellular energy has been depleted then the development of CWD fungal and yeast
forms is favoured.
The Enderlein Cycle then becomes a cycle involving the upward development of CWD’s from
the invisible protits/visible protit veil, through symprotits and other apathogenic forms, to fila,
chondrits, thecits, ascits, and other pathogenic forms to finally fuse with low valence endobiont
to produce protits and thus complete the cycle. To complete the growth phases we should
include the reversion of CWD’s to their cell wall bacterial and fungal forms during dramatic
changes to the milieu. For example, at very low oxygen status bacterial CWD’s can revert back
to their cell wall bacterial forms and in extreme circumstances this can lead to sepsis or
septicaemia and death of the living organism. Equally, if the blood pH were to reduce to 6.8, or
below, (eg. in cases of severely compromised immunity) then CWD’s of fungi and yeasts can
119
revert back to their cell wall forms resulting in fungaemia and possible death of the living
organism. The model is based on that presented earlier for mycoplasmas. This model would
explain both Enderlein’s pleomorphic cycle of bacteria and fungi as well as providing a
possible explaination for the conflict between orthodox medicine and those who support
pleomorphism and the Cellular Theory of Disease.
With this in mind it is possible to redraw the Enderlein Cycle as follows:
10.Enderlein’s Pleomorphic Cyclode Updated:
Enderlein’s Pleomorphic Cycle Updated:
Cell Wall
Deficient
Forms
11. Glossary of Enderlein terms:
Protits, protit veil = L-Forms

Symprotits, macrosymprotits = globulin proteins, L-Form bacteria, or mycoplasmas
Sporoid symprotits = mycoplasmas
Chondrits = L-Forms of rod shaped bacilli
120
Fibrin bundles = fibrin

Thrombocytes emerging from blood cells = L-forms (out of white blood cells) or
mycoplasmas (out of red blood cells)
Thrombocyte symplasts = platelet aggregates
Dioecothecits = echinocytes
Leucocytes = neutrophils, eosinophils, and basophils
Lymphocytes = neutrophils
Synascits = L-forms of bacteria, mycoplasmas, or candida spp.
Ascits = L-Forms, bacterial forms
Sclerosymprotit symplasts = pseudocrystals
Enderlein noted that most endobiont forms were observed close to the edge of a blood slide
where the blood was exposed to the air and was drying out. At this part of the slide many red
blood cells are membrane damaged, dried, or even ruptured, liberating their contents
(haemoglobin). Once exposed to the air, the haemoglobin lyses and releases globin proteins
which move by Brownian action and closely resemble what Enderlein described as chondrits
and symprotits. It is important to note that the more fragile the red blood cell membrane, the
more readily the rbc’s will lyse so it is a good indicator of the health status of the red blood
cells and, indeed, that of the patient.
In the following cycle I have attempted to summarise the work of Enderlien and include the
modern approach to his work. It is merely my attempt to bring his work into the modern era
and encompass the input of the many scientists and doctors who have contributed to the
pleomorphic approach to health and disease. As more information comes to hand I am sure that
this summary will be extended.
121
Cell Wall
Deficient
Forms
XIII. ISOPATHY AND SANUM THERAPY:

As mentioned in Section VII, above, Enderlein developed a protocol using isopathic remedies for
the treatment of disease. He set up a company in Germany, based in Hoya, to manufacture his
remedies. His successor, Herr Kehlbeck, established the Sanum-Kehlbeck company, acquired the
immunobiological company Ibica, and Sanum-Kehlbeck now produces an extended range of
isopathic and immunobiological remedies. Enderlein’s remedies were based on the pleomorphic
theory of disease and work very well, however, even if you do not adhere to his beliefs you will
find them to be a very useful tool in treating a number of health problems. The fact that they
work is in no way a confirmation that his theories are correct. The way that the isopathic
remedies are produced (from alkalizing and acidifying chemicals, bacterial antigens, bacterial
and fungal cell wall and cell membrane material, endocrine organ material, herbs, and other
substances) makes the use of them in many ways similar to inoculation which allows the immune
system to build up antibodies capable of fighting against infection by the infecting
microorganisms (Mucor, Aspergillus, and Penicillium). All three of these fungi (moulds) are
described in microbiology texts as plant pathogens that are rarely associated with human
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diseases. Penicillium notatum is the main mould from which the antibiotic penicillin was
produced and is documented as being responsible for allergies and asthma. It produces
hyperallergenic proteins called serine proteases that, when inhaled set up allergic reactions.
Aspergillus niger, if inhaled, causes aspergillosis and is also the primary cause of otomycosis.
Mucor racemosus causes allergic responses in some individuals and more recently has been
associated with sepsis in chronically ill patients (162). In all cases it is important to alkalize the
body as an essential part of treatment.
1.The 3 Cyclogenies
There are three cyclogenies (cycles) involved in Sanum therapy:
a. The Mucor racemosus cyclogeny

b. The Aspergillus niger cyclogeny
c. The Penicillium notatum cyclogeny
The basic cyclogeny is that of Mucor racemosus.
All three cyclogenies exist in a systematic way with each other.
Each cyclogeny represents development in both upward and downward directions with regards
pleomorphism. In other words, depending upon the state of the milieu, apathopenic forms may
become pathogenic and pathogenic forms may become apathogenic.
a. Mucor racemosus Cyclogeny
Mucor racemosus is found in all living mammalian cells both human and those warm blooded
animals (cattle, goats, sheep, pigs, hares, rabbits, horses, etc) that humans eat. It is present in all
blood cells and was designated by Enderlein as the endobiont.
Mucor racemosus does not exist in any non-mammalian warm blooded animals (chickens, ducks,
geese, birds) that are also eaten by humans.
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In its physiological, non-pathogenic area, the Mucor racemosus cyclogeny represents the
departure point for the Aspergillus niger cyclogeny while in its pathological area the Mucor
racemosus cyclogeny represents the departure point for the Penicillium cyclogeny.
The main functional focus of the Mucor racemosus cyclogeny is fibrinogen which, in
evolutionary terms was what made the evolution of warm blooded animals possible. Fibrinogen
is involved with all thickening and coagulation processes (particularly those of the blood) and
thus Mucor racemosus in its higher forms causes:
Thromboses
Strokes
Hemorrhoids
Varicosities
Elevated viscosity of the blood
It has also been associated with wounds, heart problems, hypertonia, general circulatory
problems and congestion.
In its highest bacterial form Mucor racemosus becomes the bacterium Leptotrichia buccalis.
Mucor racemosus forms found in Live Blood:
1. Symprotits
124
2. Macrosymprotits
3. Sporoid symprotits (mycoplasma)
125
4. Mychits
5. Thecits
126
6. Colloid thecits
7. Dioekothecits
127
8. Chondrits
9. Ascits (Leptotrichia buccalis)
128
10. Synascits
11.Symplast
129
b. Aspergillus niger Cyclogeny
Aspergillus niger is involved with a “misdirection of physiological processes within the body”. It
influences lymph vessels and glands, the chronicity of an illness, calcium balance and
metabolism, and in its highest form becomes the tuberculosis bacterium. The following organs
and systems are, therefore, subject to the Aspergillus cyclogeny:
Intestinal mucosa
Lymphatic vessels and glands
Genito-urinary tract (kidneys, bladder, uterus, ovaries, ureter)
Parametrium (testes, epididymis, prostate)
Lungs and airways
Skin and mucous membranes
Bones, tendons, septums, joints
Brain and nervous system
Tubercular and para-Tubercular problems
Aspergillus Forms in Live Blood:
1. The Oit.
130
2. Small rod forms (Mycobacterium tuberculosis)
3. Long fine thread forms.
4. “Dotted lines” – see also the fine long thread form
131
5. “Spear” shapes.
6. “Fish ribs” (drepanids)
7. Advanced Drepanid Forms
132
8. “Caterpillar” (advanced drepanid) Forms
9. Aspergillus Symplasts
c. Penicillium Cyclogeny
The Penicilium cyclogeny branches off from the pathological part of Mucor racemosus
cyclogeny and signifies the beginning of actual isopathic therapy.
It is responsible for acute inflammations and it is seen in:
All modern diseases (bacterial, viral, and fungal infections)

All acute inflammatory processes involving any organ
Chronicity of every acute relapse or further outbreak as part of a chronic disease
Asthma
Allergies
Rheumatism
133
Penicillium Forms found in live blood:
1. Coccal Bacterial Forms
2. Cell Wall Deficient Forms
134
135
3. Rouleaux
4. Erythrocyte Aggregation
5. Acanthocytes
136
6. Echinocytes
7. Schistocytes, Bite Cells
8. Fragile Leucocytes
137
9. Leucocyte Aggregation
2. Isopathy and Disease
In the human body a state of health is when the milieu is in an ideal condition that supports the
individual’s needs and is suited to the organs. If through poor diet, stress, exposure to pollutants
or artificial chemicals, etc, the milieu changes to a non-ideal condition to support ‘normal’
healthy cells, tissues and organs, then the microorganisms that are potentially pathogenic can
multiply in the body and the individual can become ill. At the ideal end of the scale (health
supporting milieu) there are sufficient (slightly excess) apathogenic microorganisms (protits,
chondrits, symprotits, and macrosymprotits) to support good health. At the other end of the scale
(poor milieu) there becomes an enormous shortage of these apathogenic forms and an abundance
of the pathogenic forms develops. This is the basis of isopathy. Many isopathic remedies are akin
to vaccines because they are manufactured from cell wall, cell membrane and other fragments of
specific microorganisms and unlike homeopathic remedies they decrease in potency with dilution
rather than increase in potency.
According to Enderlein, eating meat from warm blooded mammals introduces highly evolved
pathogenic forms into our systems and we must have an excess of the apathogenic forms in our
systems to combat this introduction.
Moderation is the key to maintaining a good milieu to support health of the individual. Eating
excess fats, sugars, carbohydrates, protein (meats and cheese), drinking too much alcohol, cow’s
milk, or carbonated soft drinks, eating too much cellulose as raw fruits and vegetables, or just
plain over-eating can lead to changes in the milieu that supports the growth of pathogenic
microorganisms.
Many drugs (medicines) can alter the milieu and they can also eliminate large amounts of the
basic (apathogenic) forms from our bodies thus increasing the relative amounts of pathogenic
forms which can constitute a danger to health. Antibiotics, antifungals, immune suppressants,
cortisone, artificial cosmetics, and long term treatments with many drugs can lead to a deficiency
of apathogenic forms.
138
Through his extensive stidies Enderlein ascertained that several human diseases were associated
with the three fungi.
Diseases of the Penicillium cyclogeny include:
Tonsillitis, sinusitis, otitis, bronchitis, cholecystitis, and several other diseases ending in –it is.
Diseases of the Mucor cyclogeny include:
Circulatory disturbances, heart disease, thrombosis, phlebitis, varices, haemorrhoids, strokes,

poor memory, lack of concentration, etc.
Diseases of the Aspergillus cyclogeny include:
Chronicity, tuberculosis, kidney and bladder problems, endometritis, orchitis, epididymitis,

brochial asthma, lymphadenitis,lymphatic congestion, colitis, diarrhea, constipation, skin
diseases, bone and joint problems, aspergillosis, otomycosis, and neuritis.
3. Chronicity of a Complaint
The chronicity of an illness is dependent upon several crucial factors:
a. the Aspergillus cyclogeny and the tubercle bacillus (Mycobacterium tuberculosis) at its
highest stage are always involved.
b. the involvement of Mucor enteralis (intestinal mucosa) most likely with candida
infection in the small intestine and depletion of normal intestinal flora.
c. The involvement of nasal sinuses, teeth, scars or inflammation of some other organ in
addition to the intestinal mucosa.
4. Organic acid specificity of Fungi
The three fungi studied by Enderlein produce specific organic acids. Mucor racemosus produces
lactic acid, Aspergillus niger produces citric acid, and Penicillium notatum produces penicillinic
acid and formic acid. For this reason, homeopathic formulas from these organic acids were
manufactured to assist with alkalization of the milieu and destruction of the fungal forms and
their reversion back into non-pathogenic (protit) forms.
5. The 4 Steps to Sanum Therapy
Dr. Konrad Werthmann has formulated a 4 step procedure to Isopathic (Sanum) Therapy that is
summarized as follows:
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For further information on Sanum Therapy you may read:
“The Four Steps of Isopathic Therapy – Prevention and Treatment” by Konrad Werthmann MD
(159).
“A Comprehensive Guide To Sanum Therapy according to Prof. Enderlein” by Gunther Weigel
(156).
“Isopathic/Homeopathic Materia Medica” by Dr. Konrad Werthmann (158).
An outline of the basic Sanum therapy which follows alkalination of the body is shown below:
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The three moulds, Mucor, Aspergillus, and Penicillium produce specific organic acids (see
earlier) that acidify the medium and stimulate the growth of the microorganism. Mucor produces
lactic acid, Aspergillus produces citric acid, and Penicillium produces penecillinic acid and
formic acid. For this reason, the appropriate homeopathic remedy for each organic acid is used in
treatment of each specific fungus/mould in order to slow the progression of their development
and assist the process of reducing the higher forms of the mould to their primitive forms and thus
restore the individual to a state of health.
Sanuvis (homeopathic lactic acid) increases mitochondrial respiration, decreases lactic acid
build up in muscle tissues and lowers blood pH.
Citrokehl (homeopathic citric acid formula) decreases citric acid levels in the body to assist in
raising pH.
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Formasan (homeopathic formic acid) relieves symptoms of allergies, rheumatism, and

inflammation.
Tartakehl (homeopathic tartaric acid) decreases tartaric acid levels in the body to assist with
raising pH in patients with candidiasis.
6.Blockages (Mochloses):
Enderlein’s Cyclode Theory was based primarily on 5 main paradigms:
a. The existence of two symbionts in all mammals, namely Mucor racemosus (the primary
symbiont or endobiont) and Aspergillus niger (the secondary symbiont).
b. The upward development of the Mucor cycle through primitive (apathogenic) forms, to
pathogenic bacterial forms to the end stage fungal forms. The fungal forms never exist
in live blood or the body until near death or death of the organism.
c. The importance of the milieu (the interstitial fluids) in maintenance of health and well
being.
d. The downward development of higher (pathogenic) forms in the cycle to lower
(apathogenic) forms.
e. The existence of blockages (mochloses) to the downward development. These
blockages stop downward development and encourage upward development, resulting
in the formation of pathogenic forms.
There are 4 main fungi that appear in the blood (and other tissues) which are deal with via
Sanum therapy, namely Mucor racemosus, Aspergillus niger, Penicillium notatum, and
Candida albicans. Others that are also used as isopathics include Mucor mucedo, Penicillium
chrysogenum, Penicillium roquefortii, and Candida parapsilosis.
The milieu is basically all interstitial body fluids including the blood, and all extracellular
fluids which encompass cerebrospinal fluid, synovial fluid, aqueous and vitreous humours, and
lymphatic fluid. Extracellular fluids make up around 75% of all interstitial fluids and the blood
of the other 25%. The milieu is mostly water with dissolved ions, proteins, and solutes. It
assists in the regulation of ionic concentration of salts, particularly those of sodium, chloride,
potassium, and bicarbonate and also helps to regulate blood pH, viscosity, osmotic pressure,
volume, and composition. Provided the milieu is well balanced and the body is in homeostasis,
the individual will be well equipped to maintain a good state of health. However, if the milieu
becomes unbalanced homeostasis of the individual will be adversely affected and the
individual will be more susceptible to infection and disease states.
Once homeostasis is disturbed through poor diet and nutrition, exposure to chemical, electrical,
and environmental toxins, etc, then there is an upward development (pleomorphism) of the
Mucor cycle to pathogenic forms which can lead to disease.
There are a number of factors that can lead to disturbed homeostasis including:
Hyperproteinaemia
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Acidification of the milieu through poor diet, inactivity, intake of alcohol, adidic drugs, etc
Dental foci – particularly amalgam fillings and any metal prostheses
Infections
Intoxications from drugs (prescribed and illicit) and environmental toxins
Heavy metals such as mercury, lead, cadmium, and arsenic
Mineral deficiencies – particularly zinc, magnesium, manganese, and copper
Trace element (selenium, germanium, manganese) content
Changes in blood viscosity due to protein levels, carbohydrate (particularly sugar) levels, etc
Poor vitamin and mineral balance
Changes in electromagnetic potential of cells
Changes in red-ox potential of cells
And, above all, poor diet
Once the milieu has been adversely affected there is usually a decrease in pH which leads to
acidification of cells and tissues which, in turn can lead to production of free radicals,
inflammatory conditions, faulty immune mechanisms (autoimmune disease), poor cellular
metabolism, premature aging, and disease states.
Heavy metals are able to set up altered electromagnetis potentials in the body and also cause
intoxications due to affects on cell membranes and as such can bring about changes in the
milieu.
Electromagnetic potential of cells can be altered by several factors including diet, dental foci,
external sources of electromagnetic fields such as mobile phone towers, electrical power
cables, transformers, and junction boxes.
The redox potential of cells is a measure of the affinity of any chemical compound for
electrons. The greater is the affinity, the greater the redox potential. When chemicals take on
electrons they are reduced and when they lose electrons they become oxidized. Free radicals
have a very high affinity for electrons and therefore have a very high redox potential. Free
radicals are generated in the body through normal physiological functions such as liver detox
pathways, mitochondrial respiration and white blood cell oxidative burst during immune
response to antigens plus external sources such as ingestion of trans fats and oxidized
cholesterol. The ideal is for cells to have a low redox potential so any measures that will lower
redox potential, for example supplementation with antioxidants, will improve the milieu and
reduce the risk of upward development of the endobiont. G.I.T. dysbiosis can also be a factor
in increasing redox potential of cells due to a build up of antigens from malabsorbed foods,
thus treating the gut is always a very good adjunct to any treatment protocol.
Any of the factors (above) that can lead to disturbed homeostasis and adversely affect the
milieu can produce blockages in the downward development of the endobiont.
Dr. Rau has outlined three major blockages in the Mucor cycle as follows:
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Blockage 1 is due to over acidification, blockage 2 due to a build up of bacterial debris, toxins,
and other debris as a result of either antibiotic treatment or treatment with Sanum Mucokehl,
and blockage 3 is due to a build up of cell wall deficient forms as a result of antibiotic
treatment or treatment with Mucokehl. All three blockages must be unblocked to assist full
downward development of the endobiont.
Blockage 1 – Acidification:
Blood pH is not static it is dynamic, changing constantly due to dietary, activity, and
environmental factors and this constant state of flux leads to the upward and downward
development of pleomorphic forms in the Mucor cycle. If the pH decreases, it favours upward
development and if it increases, it favours downward development. If the pH of any cell, tissue,
organ, or interstitial fluid becomes static then the microbes can become stuck in a
monomorphic state and are unable to develop in either direction – just as they are when grown
in culture medium – and they are not representative of the behavior of the same microbes in
living blood where they are constantly exposed to the dynamic state of blood pH which favours
pleomorphism.
pH regulation in the blood is achieved mainly through the action of bicarbonate with some
input from haemaglobin, glutamine, and sodium ions. pH is reduced through ketosis,
dehydration (caused by vomiting, low water intake, diahorrea), hyperproteinaemia, excess
intake of acidic foods such as refined sugar, animal proteins, fried foods, trans-fats, alcohol
etc.
One of the main factors involved in this process is a change in blood pH, therefore, the first
step in restoring homeostasis is to return the pH of the milieu to ideal (7.35 – 7.40). This is
done using a combination of diet, Alkala N, and possibly extra sodium bicarbonate. However,
Mucor, Aspergillus, and Penicillium produce organic acids that they secrete into their
immediate environment to acidify it and thus favour their growth ad further upward
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development. These organic acids (lactic, citric, and penicillinic – formic, respectively)
continue to acidify the milieu and if their production is not stopped, will lead to the first
blockage in the downward development. As such treatment of the first blockage is with
appropriate diet, Alkala N, and the appropriate acid reducing formula – Sanuvis for lactic acid
(Mucor), Citrokehl for citric acid (Aspergillus), Formasan for formic and penicillinic acid
(Penicillium), and Tartrakehl for tartric acid (Candida).
Once the acidification has been addressed the downward development of the endobiont is
favoured.
Blockage 2 – Bacterial debris
Antibiotic treatment for bacterial infections or treatment with Sanum Mucokehl

(spermits/bacteriophages) can lead to the production of bacterial debris, toxins, and cell wall
deficient forms (L-Forms). The former, bacterial debris and toxins leads to the second blockage
in the Mucor cycle while the latter (CWD forms) can lead to the third blockage. The second
blockage can result in the accumulation of free radicals which increases the redox potential of
cells and a built up of antigen material that can lead to the formation of antibodies by the
immune system and autoimmune complexes. The debris can be purged from the system using
Mucokehl Atox and the autoimmune complexes destroyed by modulation of the immune
system with immunobiological preparations such as Utilin or Recarcin. If there has been
Penicillium involvement then Utilin or Recarcin are also favoured but if there is Aspergillus
involvement then “S” Utilin or Latensin should also be considered along with Nigersan Atox.
Resultant free radicals can be removed using antioxidant formulas, omega-3 fatty acids, and
trace elements such as selenium (Selenokehl) and germanium (Sangerman).
Blockage 3 – Cell Wall Deficient (L-) Forms
As mentioned, above, CWD forms (L-Forms) can accumulate due to antibiotic or Mucokehl
treatment. These CWD forms only have a cell membrane so they do not have the antigens for
that bacterium. Consequently, the CWD forms are ‘invisible’ to the immune system and they
act as stealth pathogens, hiding in the cells and tissue of the body until homeostasis is
compromised at which time they can enter the plasma, develop cell walls and bring about
infections. Some CWD’s can also cause a range of diseases as the CWD form (100).
To make the CWD forms visible to the immune system they need to have an antigen attached
to their cell membrane. This is done via the haptens (Sanukehls) which are partial antigens and
become full antigens when complexed with a high molecular weight carrier protein. The cell
membrane of CWD forms act as that high molecular weight protein and once the hapten
complexes to it a full antigen is formed. The immune system is activated and then takes over
producing many B-cells containing antibodies to that antigen. After that the antigen-antibody
complexes formed are destroyed by white blood cells and the CWD forms are thus removed
from the body.
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The haptens (Sanukehls) are bacterial or fungal preparations specific to the microorganism
they are produced from. Consequently, Sanukehl Strep is used if there was a Streptococal
infection, Sanukehl Cand if there was a candida problem, Sanukehl Coli if there was an
Echerichia coli problem, Sanukehl Myc and Sanukehl Klebs for tubercular conditions, and so
on. The Sanukehls are applied topically by rubbing into the crease of the elbow. A list of
Sanukehl preparations and the underlying health problems they may assist with is as follows
(list and application from “Isopathic/Homeopathic Materia Medica” publ. Semmelweis-Institut
GmbH, Dr. Konrad Werthmann):
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Sanukehl Possible Underlying Health Problem

Acne acne, rheumatoid arthritis ________________
Brucal dysmenorrhoea, influenza, myalgia, sub-acute polyarthritis__
Cand oral cavity diseases (stomatitis, gingivitis), colitis, dysbiosis
caused by antibiotics, allergic asthma, vaginitis____________
Coli prostatitis, UTI’s, vaginitis, cyctitis, colitis, epididymitis______
Klebs resp. tract diseases (bronchitis, pleuracy, pneumonia, acute
influenza and side effects caused by antibiotics___________
Myc bronchial asthma, skin diseases (rhinitis, psoriasis, lupus,
keratitis), conjunctivitis, duodenal ulcers, cystitis, otitis_____
Prot intestinal tract diseases (gastroenteritis, peritonitis,
dysbiosis from antibiotics), lung diseases, dysbiosis, Herpes__
Pseu skin infections, keloids, burns, autoimmune diseases,
fibromyalgia, chronic bronchitis, oedema, Menierre’s________
Salm impaired growth, chronic pancreatitis, gastroenteritis,
celiac disease, rheumatic fever___________________________
Serra nocosomal infections from Serratia enteridis_______________
Staph skin infections (folliculitis, impetigo, acne), urogenital staph___
infections, meningitis, osteomylitis, otitis, mastoiditis________
Strep alopecia, eczema, empyema, cardialgia, pericarditis,
chronic polyarthritis, mastitis, migraine____________________
7.Prescribing Sanum:
There are different ways of prescribing Sanum, however, we have put together a Flow Chart
that describes the basic principles of prescribing in a simplified form. The Flow chart follows:
Sanum Flow Chart (Australia)

1. Alkalise to restore ideal Blood pH (7.40): Remove Blockage 1
• Alkala-N
• Sanuvis (Mucor)
• Citrokehl (Aspergillus)
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• Formasan (Penicillium)
• Tartakehl (Candida)
• Alkalising Diet
2. Treat with Penicillium formulas: Reduce inflammation/infection
a. Staph or Strep Infection Notakehl, Sanukehl Staph/Strep
b. Dysbiosis of the G.I.T.
Gastritis
Colitis G.I.T. Fortakehl, Sanukehl Coli, Prot, Salm
Pancreatitis
Gastric Ulcers if candidiasis Pefrakehl, Sanukehl Cand
c. Prostate/Vaginal mycosis Exmykehl, Sanukehl Cand
Intestinal mycosis if candidiasis Albicansan, Sanukehl Cand
d. Viral Infections
Viruses all forms Quentakehl, Sanukehl Strep, Prot
e. Infection
Urinary Tract UTI’s and Kidney Notakehl, Sanukehl Strep, Staph, Coli, Cand
f. Sexual Infection
Chamydia Vaginal and Testicular Notakehl, Fortakehl, Sanukehl Myc, Coli
Pelvic Inflammatory Disease
g. Yeast Problems (Candidiasis) or if Antibiotics were used:

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Candidiasis of the G.I.T.
Mouth Ulcers
Cystitis Pefrakehl, Fortakehl, Sanukehl Cand
Proctitis
Athlete’s Foot
h. Candidiasis of Soft Tissues
Mouth, Gums
Vagina Albicansan, Exmykehl, Sanukehl Cand
Urethra
*Note: addition of the Sanukehls early in treatment can accelerate healing
3. The Basics (Mucokehl & Nigersan) Down Regulate Bacterial Forms
a. Mucor racemosus (Flow and Stasis):
Circulation – Veins/Arteries
Haemorrhoids
Blood Clotting/Thromboses
Heart Mucokehl, Utilin
Thrombocytosis/Thrombocytopaenia
Anaemia
b. Aspergillus niger (“Degenerative” Problems):
Lymphatics
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Bones/Joints/Calcium Balance
Lungs/Bronchi/Asthma Nigersan, Ruberkehl, “S” Utilin
Tubercular Problems
Genito-Urinary Tract
4. Excretion/ Remove Wastes: Remove blockage 2 (Cell Wall Debris etc.)
Mucor racemosus Mucor Atox
Aspergillus niger Nigersan Atox
5. Immune Modulators: Modulate Immune System
Mucokehl use: Utilin or Recarcin
Nigersan use: “S”-Utilin or Latensin
Notakehl use: Utilin
Fortakehl use: Recarcin, Leptucin
Quentakehl use: Leptucin, Utilin, Recarcin
Mucedokehl use: Utilin, Recarcin, or Leptucin
Pefrakehl use: Arthrokehlen A or U or Leptucin
Albicansan use: Arthrokehlen A or U or Leptucin
Ruberkehl Utilin or “S” Utinin
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6. Organ Treatments: Support organs that may have been affected
Liver & Spleen Problems: Pinikehl, Mucedokehl
Lung, Digestive Tract, Polyarthritis Problems: Larifikehl, Sanukehl Brucel
Upper & Lower Respiratory Tract: Ruberkehl
Neurological, Lymphatic Problems Mucedokehl
7. Sanukehls (Haptens): Remove Blockage 3 (CWD Forms)
Rheumatoid Arthritis Acne
Dysmenorrhoea, influenza, myalgia, polyarthritis Brucel
Oral cavity diseases (stomatitis, gingivitis), colitis, dysbiosis caused by
antibiotics, allergic asthma, vaginitis Cand
Prostatitis, UTI’s, vaginitis, cystitis, colitis, epididymitis Coli
Respiratory tract diseases (bronchitis, pleuracy, pneumonia, acute
influenza), side effects of antibiotics Klebs
Brochial asthma, skin diseases (rhinitis, psoriasis, lupus, keratitis),
conjunctivitis, duodenal ulcers, cystitis, otitis Myc
Intestinal tract diseases (gastroenteritis, peritonitis, dysbiosis from
antibiotics), lung diseases, dysbiosis, Herpes Prot
Skin infections, keloids, burns, autoimmune diseases, fibromyalgia,
chronic bronchitis, oedema, Menierre’s disease Pseu
Impaired growth, chronic pancreatitis, gastroenteritis, celiac disease,
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rheumatic fever Salm
Nocosomal infections from Serratia enteridis Serra
Skin infections (folliculitis, impetigo, acne), urogenital staph infections,
meningitis, osteomylitis, otitis, mastoiditis Staph
Alopecia, eczema, empyema, cardialgia, pericarditis, chronic
polyarthritis, mastitis, migraine Strep
Mycosis of the hair, skin, nails, tinea, trichophytosis, impaired skin
function, hair loss Trich
8. Glandulars: Support Glands that nay have been affected
Disorders of growth & development, all degenerative processes in the
lumbar vertebral column Thymokehl
Recurrent & chronic inflammation, gastrointestinal diseases, chronic
hepatitis, tonsillitis Rebas
9. Botanicals:
Adaptogenic effect on unbalanced body functions, diabetes mellitus
hypertonia, obesity, immunostimulant Grifokehl
Impaired immune defence, prostate adenoma Fomepikehl
Drug detoxification (from drug abuse), cerebral ischaemic attack
nervous excitability, muscle spasms, organs & blood vessels, migraine,
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nervous disorders of the intestines Muscarsan
Cardiac weakness, low blood volume, hypertension, high sodium,
nervous heart from smoking, arteriosclerosis, anticipatory anxiety,
bleeding & profuse blockage of the uterine region Strophanthus
10. Polysans Treat for heritable and multi microorganism infections
Polysan A Complaints due to aging, Glandular & Metabolic disorders,
Arteriosclerosis, Hypertension, Cardiac Infections & Heart disease,
Nervous disorders, Paradontosis, Periodontosis, Prostatic diseases.
Polysan D Focal Infections – Teeth, Tonsils, Sinuses.
Polysan Dx Focal Infections – Teeth, Tonsils, Sinuses.
Polysan E Inherited Toxins – especially those of a leutic nature,
Insomnia, Memory disturbances, Joint disorders, Psychosomatic
disorders, Anxiety, Irritability, Depression, Hypochondria, Lyme disease,
Chronic fatigue, Fibromyalgia.
Polysan G Influenza, Angina, Festering of sores & wounds, Blood
poisoning, Feverish diseases, Respiratory diseases, Sore Throat, Boils.
Polysan K Circulatory disturbances, Venous congestion, Lymph
congestion, Colic, Allergies (Asthma, Hay Fever), Varicous Veins.
Polysan M Malaria, Babesiosis, Dengue fever, Yellow fever, St Louis
Encephalitis, West Nile virus.
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Polysan Om Circulatory disturbances, Venous illness, Allergic illnesses
(use with Polysan A & K), Treatment of pain.
Polysan R Rheumatism, Gout, Neuralgia, Elimination of Uric acid,
Rheumatism of tubercular origin, Sciatic pain, Sciatic Neuritis.
Polysan T Tuberculosis (Latent & Masked form), Asthma, Eczema,
Rheumatism, Migraine, Scrofula (Lymphadenitis).
Wertmann’s 4 steps to Sanum Therapy can be extended to a 7 step programme designed to

restore health to the individual. It follows:
7. The 7 Steps to Restoring Health to the Individual
Step 1 – The milieu
The first step is always to promote homeostasis by returning pH, temperature, blood glucose, etc
to normal levels. This is done through Sanum by buffering the blood with bicarbonate and/or
citrate using products such as Alkala N, Sanuvis, Citrokehl, and Formasan. The pH of blood is
maintained at around 7.4 primarily through the buffering action of bicarbonate which is regulated
through carbon dioxide produced through respiration and the kidney’s ability to convert it to
bicarbonate anions. Other anions that affect blood pH include citrate, phosphate, ammonium,
acetoacetate, hydroxybutyrate, and sulphate. These anions usually lead to acidosis until they are
eliminated by the kidneys. By providing the body with extra bicarbonate we allow the body to
more rapidly restore normal pH and provide the blood with great buffering capacity to maintain
that ideal pH. This process is usually undertaken for 7 – 10 days to restore the pH of the milieu to
ideal (homeostasis) and is undertaken in conjunction with an alkalizing diet.
It is essential that the diet is addressed in order that ideal pH is maintained throughout a treatment
protocol. A simple diet that will achieve this end is to make high protein foods ⅟3, or less, of any
meal and the other ²/3 alkaline foods such as vegetables, salads, and fruits. Wertmann eliminates
all flesh foods, tea, coffee, all dairy, and a range of other acid foods altogether from the diet
which is fine but is probably not so conducive to patient compliance. Why remove dairy? There
is a wealth of research data correlating the intake of dairy to both type-1 and type-2 diabetes and
heart disease, however, in avoiding all dairy we may be throwning out the baby with the bath
water! Recent research by Professor Bob Elliott at the University of Auckland, NZ, has shown
that this correlation is strong when considering the milk protein β-casein A1 present in cow’s
milk from cows that produce this protein. The β-casein A1 is apparently fragmented during
digestion to produce a secondary product, β-casomorphin 7, which has also been linked with
factors involved with heart disease such as platelet aggregation and LDL oxidation. Extending
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this work, Dr. Corran McLachlan, at the NZ Dairy Corporation, showed that another milk protein
β-casein A2 (which is present in milk from certain breeds of cow) is not fragmented during
digestion to form the β-casomorphin 7 that causes heart disease, diabetes, and other illnesses.
Perhaps a more sensible approach would be to only allow dairy from the β-casein A2 producing
cows rather than eliminate all dairy. Interestingly, Enderlein advocated a lacto-vegetarian diet.
Step 2 - Treat infections and/or inflammatory conditions
Wherever there is evidence of infections or inflammatory processes these must be treated first.
Sanum offers a range of products for this purpose including Notakehl, Exmykehl, Fortakehl,
Pefrakehl and Quentakehl. Immune modulators such as colostrum, zinc, astragalus, Echinacea,
vitamin D3, etc and natural anti-inflammatories such as omega-3 fatty acids (EPA), ginger,
turmeric, onions, garlic, licorice can also greatly assist in this regard. The importance of treating
the Penicillium first is that once down regulated the lower forms of Penicillium enter the
bacterial phase of the Mucor cycle and then have to be dealt with to down regulate the Mucor
cycle to the apathogenic forms.
Step 3 – Support Beneficial Microflora (the Basics)
The beneficial microflora are colloid preparations of the endobiont that undergo sexual union
with the pathogenic microorganisms leading to their destruction and a return to spermits and
microchondrits (apathogenic endobiont). Once this process takes place there is a release of waste
products and toxins from the breakdown of these microorganisms that need to be removed from
the body via the normal elimination organs (bowel, liver, kidney).
Beneficial microflora are found in the apathogenic phase of Enderlein’s cycles and Sanum
preparations of these microorganisms (Mucokehl and Nigersan) are used in this regard. In some
cases the bacterial and fungal toxins liberated are not able to be removed by the immune system
in their current form so the use of antibody preparations of Mucokehl (Mucokehl Atox) and
Nigersan (Nigersan Atox) are used to purge these fragments. If CWD forms of the bacteria
accumulate through the process of treatment with either antibiotics or the sanum basics, then
polysaccharide fragments (haptens) from bacteria, yeasts, and fungi that are able to bind with the
cell membrane of the CDW form to produce antigens recognized by the immune system which
can be eliminated accordingly. The hapten products include the Sanukehl range which covers a
large range of microorganisms.
Step 4 –Modulating the Immune System & Improving Microcirculation
Once the body is returned to ideal pH it is necessary to modulate the immune system in order to
allow it to remove breakdown products from the destruction of bacteria and fungi during a
treatment protocol. The use of immune modulators such as isopathic remedies (Latensin,
Recarcin, “S” Utilin, and Utilin), colostrum, zinc, vitamin C, etc should be supplemented to
improve immune activity especially as most pathogenic bacteria grow best at ideal blood pH.
Microcirculation can also be stimulated with Sanum products such as Mucokehl and supplements
such as omega-3 fatty acids, vitamin C, and bioflavonoids.
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Step 5 - Remove (detoxify) lifestyle and environmental blockages
The Sanum products Mucokehl Atox and Nigersan Atox are particularly suitable for this purpose
along with supplements that support liver and kidney function, including potent antioxidants that
promote liver detoxification (sulfurofane, superoxide dismutase, catalase, zinc, copper,
manganese, vitamins A, C, E, glutathione, cysteine, CoQ10, carotenoids, bioflavenoids,
selenium, pycnogenols, etc).
Step 6 - Assist in repairing organs and tissues
For the purpose of aiding the body to repair damage to organs and tissues Sanum offers several
products. They include the glandular remedies (Chysocor, Rebas, and Thymokehl), botanical
remedies (Cervikehl, Ginkgobakehl, Leptospermusan, Usneabasan, Okoubasan, Relivora, and
Stophanthus), excretion remedies (Mucokehl Aand Nigersan Atox) and the chelation remedy
Pleo Chelate. A good multivitamin/multimineral supplement and healthy eating regime are also
important to support organ and tissue repair.
Step 7 – Supplementation
Where necessary it may be a requirement that you add in specific supplements (see other steps,
above) to support the Isotherapy protocol. These supplements will vary depending upon the
treatment and the individual’s specific requirements.
XIV. CATEGORIES OF DFLBM OBSERVATIONS
DIGESTION
1. Protein Linkage rbc's linked into chains Poor protein digestion

2. Rouleau rbc's like stack of coins Poor digestion/assimilation
3. Rbc Aggregation rbc's clumping Poor digestion/assimilation/Chronic problem
CIRCULATION
1. Platelet Aggregation platelets clumping Low omega-3's

2. Spikules needle-like structures Liver stress
3. Protoplasts crystal aggregates Early plaque formation
4. Atherosclerotic Plaque opaque globules Hardening of arteries
5. Chylomicrons small motile dots Fat droplets
IMMUNE SYSTEM
1. Increased Eosinophils more than 3% of wbc's Allergies

2. Hypersegmented PMN's more than 5 lobes Acute infections
3. Neutrophil Viability amoebic movement Active, healthy wbc's
4. L-forms grey, dust-like haze Bacterial/fungal infections
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5. Fungal forms bud forms/fungal hyphae Candida/Mucor/Aspergillus

6. Rod forms rod shaped microbes Bacterial infections
7. Mycoplasmas round, motile microbes Infections/arthritis/CFS
CRYSTALLINE STRUCTURES
1. Cholesterol bright white crystals Liver/poor diet

2. Uric acid yellow, square crystals Poor kidney elimination
3. Red crystals red, amorphous shape Leaky gut
RED BLOOD CELLS
1. Anisocytes variation in size anaemia

2. Poikilocytes variation in shape toxins present
3. Ovalcytes oval shaped rbc's anaemia/low magnesium
4. Microcytes small rbc's low iron
5. Macrocytes large rbc's low B12/folic acid
6. Target cells dark ring in pale rbc low iron/anaemia
7. Pencil Cell long, thin rbc's haemolytic anaemia
8. Acanthocyte scalloped edge on rbc detoxification
9. Echinocyte spikes on surface of rbc inflammation/ROS
XV. MICROBIAL INDICATIONS FROM THE BLOOD:

Inflammation (Penicillium cycle):
Rouleaux
Red Blood Cell Aggregation
Echinocytes
Fragile Neutrophils
Acanthocytes
Fragile Erythrocytes
Elevated White Cell Count
Coccal Bacterial Forms (particularly Streptococcus and/or Staphylococcus)
Activated T-cells
Excess lymphocytes
Yeast forms
Fungal forms
Bacterial forms
Circulation (Mucor racemosus cycle):
Excess Chylomicrons (empty stomach)

Fibrin Spikules
Cholesterol Crystals
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Platelet Aggregation
Erythrocyte Aggregation
Lipid Ribbons
Heterogeneous Plaque
Leptotrichia buccalis Rod Forms
Fungal Mycelia
Airways, Mucous Membranes, Physiological problems (Aspergillus niger cycle):
Protein Linkage
Rouleaux
Excess Neutrophils
Excess Eosinophils
Excess Basophils
Excess Lymphocytes
Echinocytes
Acanthocytes
Ascits (Tubercule bacilli)
Aspergillus drepanids
Fungal Mycelia
XVI. DFLBM OVERVIEW:

1. Rbc observations.
Note: shape, colour, degree of crenation, size, and membrane integrity.
2. Wbc observations.
Note: numbers, size, kind, activity, segmentation, membrane integrity.
3. Platelet observations.
Note: size, numbers, extrusions (spikules).
4. Crystals and pseudocrystals.
Note: Colour, size, numbers.
5. Microbial observations.
Note: size, colour, type, mobility.
6. Lipid observations.
158
Note: size, complexity, motility, crystal content, shape.
XVII. LBA MORPHOLOGY DRAWINGS:

The following are drawings of the general morphology (size, shape. Etc) of all of the cells and
other elements seen in the peripheral blood. They are to act as a guide to what is actually observed
in the blood. Some information relating to these morphological forms is also included.
159
160
161
162
163
164
165
166
167
168
169
170
171
172
173
XVIII. DFLB Observations & Possible Indications

----------------------------------------------------------------------------------------------------------------------------------------------
OBSERVATIONS POSSIBLE INDICATIONS
I. Red Blood Cells
Protein Links. Alkaline profile

Poor digestion/assimilation
Myelophthistic anaemia
Myelofibrosis
Rouleau Formation. Poor digestion/assimilation of proteins and fats.

Hyperproteinemia.
Reduced oxygen transport.
Fatigue, lethargy
Inflammatory processes
Multiple myeloma.
Polymyalgia rheumatic
Temporal arteritis
Red Blood Cell Poor digestion/assimilation of proteins and fats.

Aggregation Chronic condition.
Degenerative condition.
Calcium/phosphorus/pH off.
Severe Allergies
Inflammatory processes
Smoking, emphysema.
High caffeine.
Potential for thrombosis
Viral infection.
Rbc's smaller than Poor iron assimilation.

normal. Anaemia.
Low haemoglobin.
Bone marrow problem.
Menses
Rbc's larger than Poor iron assimilation.

normal. Calcium/phosphorus/pH off.
Deficiency in vitamins B6, B12, A, C, and folic acid.
Mainly B12 deficiency.
Rbc's oval shaped Low magnesium.

Radiation/Chemotherapy damage.
Elliptocytosis
Iron deficiency anaemia
Rbc membrane Detoxifying.

damage,bottle tops Environmental/chemical allergies.
Chronic fatigue.
Epstein-Barr Virus.
Cytomegalovirus.
Yeast Infection.
High cholesterol in rbc membrane
Rbc spikes, Chronic condition.

crenation,shadows Degenerative condition.
Low minerals (Mg,Cr,Se,Zn)
Muscle soreness.
Fatigue.
Virus activity.
Chemotherapy/Radiation therapy
174
____________________________________________________________________________
OBSERVATION POSSIBLE INDICATION
Rbc's fragile, Malignant Hypertension

broken,membrane Hemolytic uremic syndrome
fragments. Liver & spleen malfunction.
Artificial valves, stents, grafts
Rbc fragments cont. Thrombotic purpura

Pre-eclampsia
Meningococcal sepsis
Rbc dots white, Sugar intolerance/reactive hypoglycaemia.

off-centre,misty. Hypoglycaemia.
Rbc patterns, Parasite infection.

crescents. Headaches, migraine.
Rbc Teardrop shapes Myelofibrosis

Thallassemia minor
II. White Blood Cells.
Wbc's fewer than Bacterial infection.

normal. Immune system suppressed.
Wbc's more than Candida infection.

normal. Leukemia (if blasts).
Activated immune system.
Viral infection.
Polymorphonuclear Immune system sluggish/suppressed.

Leucocytes- few Acute infection.
granules,inactive. Toxic chemical exposure.
Hereditary factors
PMN's Acute infection (cocci, spiroketes, viruses, parasites).

hypersegmented Low vitamins B12 and/or folic acid.
Environmental/chemical poisoning.
Rapidly growing neoplasms
Wbc's irregular, Chronic condition.

small moving dots, Bone marrow problem.
fragile.
Eosinophils Allergies, IgG, IgE.

excessive Detoxifying from prescription drugs.
Lung problems.
Chemotherapy damage.
Parasites.
Yeast infections.
Basophils Environmental allergies IgE.

excessive Cataracts.
Watery eyes.
Dark circles around eyes.
Runny nose, sinus, cold, flu.
Lymphocytes Bacterial infection.

excessive Immune system active.
Environmental chemicals.
Virus activity.
175
Leukemia (if blasts).

T- & B- cell problems.
_____________________________________________________________________________
OBSERVATIONS POSSIBLE INDICATIONS
________________________________________________________________________________________________________________
Lymphocytes low Chemotherapy.

Virus activity.
HIV/AIDS.
T- & B- cell problems.
Lymphocytes Virus activity.

cytoplasm damage
Enlarged T-cells Immune system activated.

Severe Infection/inflammation.
Monocytes high Bacterial infections.

.>4% Protozoan infection.
Rickettsial infection.
Tuberculosis.
Subacute bacterial endocarditis.
Macrophages Immune system active.

active 〉 3% Severe infection.
Lupus erythematosis.
Haemolytic anaemias.
Band neutrophils Acute trauma, blood loss.

> 3% Appendicitis.
Severe inflammation.
Wbc's viability low Immune system suppressed.

Bacterial infection.
Chemical agent toxicity.
Hereditary defect of immune system.
III. Platelets
Platelet Excess fats in blood stream.

aggregation High caffeine.
Low vitamin C.
Potential blood clotting problem.
Thrombocytopaenia.
Spikules in serum Detoxification.

Liver stress.
Excess use of drugs, alcohol.
Dysbiosis.
Lipid Ribbons Poor fat metabolism.

Elevated serum cholesterol.
Poor liver function.
Atherosclerotic Atherosclerosis.
plaque Excess saturated fats in diet.
Excess smoking.
Excess fats in bloodstream. Chylomicrons
Protoplasts Weakened immune system.

excessive Potential plaque formation.
176
---------------------------------------------------------------------------------------------------------------------
OBSERVATION POSSIBLE INDICATION__
IV. Crystals
Cholesterol Elevated LDL cholesterol.

crystals Vitamin C low.
Diet low in soluble fibre.
Diet high in sugar.
Diet high in saturated fats.
Uric acid crystals Acid profile.

Poor kidney function.
Arthritis/gout.
Dehydration.
Under exercise.
Red crystals Malabsorption.

Bowel dysfunction ((toxicity)
Poor circulation.
Brown Potential for melanomas.
Blue crystals Pesticides toxicity.
Green crystals Pharmacological drugs.
V. Microbiology
L-forms Scleroderma
Tuberculosis
Various cancers
Immune system suppressed
Sarcoidosis
Rheumatoid arthritis
Chronic fatigue syndrome
Lyme disease
Antibiotic treatment
Parkinson’s disease
Pulmonary thrombosis
Multiple sclerosis
Inflammatory bowel disease
Lupus erythematosis
Diabetes mellitus
Candida buds Candida infection.

Antibiotics treatment.
Bacterial infection
Candida fungal Candidiasis.

Broncho-pulmonary infections
Immune system suppressed
Secondary intestinal infections
Deep blood-borne infections
Rod Forms Bacterial infection.
177
Mycoplasmas Gulf War Syndrome

excessive Arthritis.
Pneumonia.
Genito-urinary tract infection.
Neorological diseases.
OBSERVATION POSSIBLE INDICATION
Chronic fatigue syndrome
Mucor racemosus Thromboses

Strokes
Hemorrhoids
Varicosites
Aspergillus niger Intestinal mucosa problems

Genito-urinary tract infections
Parametrium problems
Lung & airways problems
Skin and mucous membrane problems
Bones, tendons, septums jonts
Brain & nervous system
Penicillium Acute inflammatory problems
**Remember at all times:
What you see (observations) may indicate a number of possible problems or potential
problems. Always question the patient to ascertain what the actual problem may be and treat
according to information you get from the patient.
These tests are screening tools to assist you with assessing the state of health of a patient.
They are not diagnostic tests.
XIX. Live Blood Microscopy REFERENCES:

The principle references used in preparing these notes follow. Most of the general information
on haematology of blood has been sourced from:
a. “Essential Haematology” eds Hoffbrand, A.V. & Pettit, J.E. (1993) publ. Blackwell
Scientific Publications. ISBN 0-632-01954-9 (BSP)
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9631819-4-7.
c. “Haematology” eds Linch, D. & Yates, P. (1986) publ. Churchill Livingstone. ISBN 0-
443-02842-7.
d. “Principles of Anatomy & Physiology” eds Tortora & Anagnostakas
178
e. “Clinical Nutrition: A Functional Approach” eds Bland, J.S., Costarella, L., Levin, B.,
Liska, D., Lukaczer, D., Schilz, B., & Schmidt, M.A. (1999) publ. The Institute for
Functional Medicine.
Enderlein’s cyclogenies and bacterial research is from:
“Bacteria Cyclogeny” by Dr. Günther Enderlein. ed Dr. A. Baum, (1981) publ.

Enderlein Enterprises Inc.,
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1

DARK FIELD LIVE BLOOD

Notes compiled by:

X. Microbes in Peripheral Blood – A Modern Perspective 108

XIII. Isopathy and Sanum Therapy 121

2. Isopathy and Disease 137

XIV. Categories of DFLBM Observations 155

Food for Thought:

“the mind is like a parachute – it only works when it is open” Anon

I. LIVE BLOOD MICROSCOPY - HISTORY:

All microscopy depends upon two main factors:

1. Resolution (the ability to differentiate two objects close together)

II. DARK FIELD LIVE BLOOD MICROSCOPY

III. THE BLOOD

IV. CONSTITUENTS OF BLOOD

a. The Red Blood Cells

b. The White Blood Cells

White blood cells consist of approximately 60 - 70% neutrophils, 20 - 30% lymphocytes, 2 - 4%

ii. Agranular Leucocytes

(4). Plasma cells

Platelets have a very short life span of some 9 to 12 days.

V. BLOOD CELL FORMATION (HAEMATOPOIESIS)

Courtesy of “Principles of Anatomy and Physiology” eds Tortora & Anagnostakis

1. Red Blood Cell Production (Erythropoiesis):

2. White Blood Cell Production:

Thrombocytes are produced by the differentiation of megakaryoblasts into megakaryocytes which

VI. BLOOD DISORDERS

Microcytic anaemia is due to iron deficiency, Thalassaemia, chronic disease, or sideroblastic

2. Infectious Mononucleosis (Glandular Fever)

Scepicaemia (bacteraemia) is a bacterial infection in the blood usually as a result of a severely

VII. THE HISTORY OF THE THEORY OF DISEASE

In 1762, M. A. Plenicz, a Viennese physician published a germ theory of infectious disease. He

Claude Bernard (1813 – 1878)

Louis Pasteur (1822 - 1895)

Antoine Béchamp (1816-1908)

It is argued by Douglas-Hume (40) that Béchamp’s microzymas may, in fact, be chromatin as he

Günther Enderlein (1872-1968)

Wilhelm Reich (1897-1957)

Gaston Naessens (1924-2005)

Microzymas are described as:

a. Non-perishable and indestructible

The two symbionts described by Enderlein are believed to be transmitted diaplacentally to

k. The basit – a coccal bacterial form with 1 – 2 nuclei.

o. The thrombocyte – a mychit with 2 – 8 nuclei. He also described thrombocyte symplasts

s. Sclerosymprotitsymplasts are most likely pseudocrystals.

a.The Germ Theory:

i. assumes that the milieu, or terrain, of the body is unimportant

b.The Cellular Theory:

What is important to remember is:

IX. CONTROVERSIES IN LIVE BLOOD ANALYSIS

The two main controversies in Live Blood Microscopy are:

1. Where do microorganisms present in blood originate from? and

1. Where do microorganisms present in the blood originate?

However, Enderlein did accomplish several things:

2. Do candida spp. exist in the blood of ‘healthy’ individuals?

According to mainstream medicine Candida albicans is only found in the blood of

X. DARK FIELD LIVE BLOOD MICROSCOPY

3. Observations and Recommendations

a. Normal, healthy blood

b. Abnormal Red Cell Observations

ii. Rouleaux Formation

iii. Erythrocyte aggregation

Treatment is by supplementation with a well balanced multivitamin, multi-mineral, formula which

(3).Acanthocytes - membrane damage/bottle tops