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What Really Makes Us Sick? The Terrain or the Germ? Part II

Introduction

In part I of “What Really Makes Us Sick? The Terrain or the Germ?”, we discussed the history of the germ and terrain theory, as well as some of the foundational principles of the terrain theory. In part II, we will introduce the concept of pleomorphism and explore some alternative reasons why we actually become sick. If you haven’t already read part I of this blog, it is important to do so, to be able to understand the topics discussed part II.

Monomorphism VS Pleomorphism

When Louis Pasteur proposed the germ theory in the 1850’s, he was convinced that all micro-organisms, such as bacteria had a definite and unalterable function, a fixed size and shape and that they were derived from an identical cell of the same lineage1. He argued that each pathogenic species of bacteria caused one specific disease and that they must be ‘caught’ from our external environment1. According to Pasteur, bacteria with these specific characteristics have only “one form” and are therefore considered to be “monomorphic”2. Around the same time, Pasteur's contemporary and adversary, Antoine Béchamp proposed an alternative theory that bacteria can have “many forms” and are therefore “pleomorphic”2.

The modern day definition of pleomorphism states that whilst microorganisms and cells possess the ability to assume several different sizes and shapes3, modify their internal structures (such as mitochondria)4 and alter their reproductive capabilities5, they do not possess the capability to transform in to other species or cell types. This modern understanding is very different to the original theory proposed by Antoine Béchamp which is that micro-organisms of all forms are derived from immortal, indestructible, ultra-microscopic, subcellular living particles called microzyma (which are introduced in Part 1)1.

Béchamps work on pleomorphism also lead him to believe that the micro-organisms that arise from microzyma are able to spontaneously transform in to other micro-organism, depending on their surrounding environment (ie the terrain or milieu intérieur)6. Evolutionary and molecular biologist Ford Doolittle said that “distinctions of species among the bacteria is denied in pleomorphism, and all forms are regarded as modifications of a single species or whatever else it may be called, and these modifications can be transformed by cultivation into one another reciprocally”6. Given these statements, it would be reasonable for one to ask the questions “Why haven’t any other scientists ever been able to replicate Béchamps work and find microzyma?” and “How can pleomorphism have any scientific validity if microzyma have never been proven to exist?”.

When looking through the literature, there are a considerable number of instances where scientists have described unknown microscopic particles present in human blood, that have characteristics very similar to microzyma. For example, in 1925, entomologist, zoologist and microbiologist Günther Enderlein described ultra-microscopic, sub-cellular particles in healthy human blood in his book Bacteria Cyclogeny7. He observed that these sub-cellular particles could develop in to other types of cells, depending on the environment they were exposed to7. Enderlein named these particles “endobionts”7,8 and proposed that they are the most basic particle that all life stems from7. In 1933, bacteriologist Professor John Ledingham described microscopic pleomorphic bacteria, that closely resembled a virus. He observed these organisms changing their size and shape and giving rise to other complicated structures9. His findings were highly controversial and were met with scepticism because they challenged the conventional view of monomorphism9.

Decades later in the 1960’s, microbiologist Gaston Naessans identified indestructible, ultra-microscopic, sub-cellular particles in healthy human blood. He named these particles “somatids”8,10 and just like Béchamp and Enderlein before him, confirmed that somatids could develop in to different micro-organisms depending on their external environment10. Neassens also stated that somatids are “precursors of DNA” and that their discovery brings a “brand new understanding to the very basis of life”10. Rather than Enderleins’ and Naessens’ work being acknowledged by the scientific community and given the further rigorous investigation their findings deserved, they were criticised and persecuted, and their work was pushed into obscurity. In science, when something is discovered that challenges the main stream understanding, it should be investigated further so that it can be proven or disproven, rather than being labelled non-sense, especially when several scientists are observing the same thing.  

If it is true that microzyma are present in the blood, and microzyma give rise to micro-organisms, then how is blood sterile? It has been a long-held belief that human blood is sterile and that bacteraemia or sepsis (blood poisoning) would occur if a person’s blood was contaminated with bacteria11. Some readers may be surprised to learn that the blood of healthy individuals is far from sterile. This is evidenced by the work of Ernest Villequez in the 1950’s and 1960’s, who discovered what he believed to be tiny parasites resembling cell wall deficient bacteria in human blood12. Could it be that these tiny parasites were in fact microzyma, endobionts or somatids? Then there is the considerable bodies of work published by scientists such as Giuseppe Tedeschi13–15 and Phyllis Pease16–18 who found that bacteria is continually present in healthy and diseased people’s blood8. A recent study published in 2019, found two species of bacteria present in the blood of healthy people, distinct from any other previously identified species19. Despite this evidence, there is very little discussion in the literature about how bacteria can enter in to the blood stream without causing sepsis and what their role is whilst in the blood.

In 1978, Bartlett and Bisset concluded that 30% of all healthy individuals have gram-positive L-form bacteria in their blood streams. Interestingly, they describe this bacteria as not having a cell wall and resembling tiny, microscopic parasitic like particles that are commonly found inside human red blood cells20. Then in the year 2000, virologist Dr. Lida Mattman described her findings of a particularly fascinating process in her book Cell Wall Deficieint Forms: Stealth Pathogens21. Dr. Mattman found what she believed to be tiny parasites present within human red blood cells, that when exposed to heat, would change their form in to a substance “indistinguishable from haemoglobin”21. Interestingly, Mattman specifically referenced the work of Tedeschi, Bartlett and Bisset due to the similarity of their results. Were the tiny, microscopic parasitic particles these scientists were observing just the microzyma, endibionts and somatids that Béchamp, Enderlein and Naessans discovered decades prior?

This evidence suggests that blood is in fact not sterile. So where do these micro-organisms come from? A recent review suggests that the blood has its own microbiome and that bacteria might be transient residents in the blood, translocating from tissues such as the skin and gastrointestinal epithelium22. If this is the case, then why are only certain types of bacteria found in the blood? Surely all types of bacteria from the gastrointestinal tract would be constantly entering the blood stream if this is the case. How can only selective bacteria translocate in to the blood? If bacteria were truly translocating from the skin and the gut, then people would be falling ill with septicaemia all the time.

In 2002, a research team published their findings in the Journal of Clinical Microbiology on pleomorphic microorganisms existing in the blood of healthy people. The authors described these organisms as highly organised entities, distinctly different from random cellular debris. Interestingly, their attempts to grow these microorganisms in the laboratory failed, suggesting that these organisms are only viable whilst circulating in the blood stream23. Could it be that what these scientists were observing were microzyma and the various organisms that had developed from them?

Experiments Upon Volunteers to Determine the Cause and Mode of Spread of Influenza

In part 1 of this blog, I referenced a 1919 paper by Milton Rosenau, published in Journal of the American Medical Association titled Experiments Upon Volunteers to Determine the Cause and Mode of Spread of Influenza”. In this paper, Rosenau mentioned another study with similar methodology and results that had been conducted around the same time as his study24. Since learning of this other study, I immediately conducted a search to find it, and after many months I finally located it. Much to my surprise, the study that I found is a 109 page document containing the results of three separate experiments. The attached image above is a picture of the front page of the document. 

The series of three experiments were undertaken by the US Navy and US public health service in an attempt to identify the cause of the Spanish flu. These weren’t just any ordinary experiments. They had the highest-ranking Navy and Government officials and departments involved. There were approximately 60 medical doctors, surgeons and surgeon generals, chemists, bacteriologists and professors from places like John's Hopkins University, Boston University and the University of Missouri. All three experiments were overseen by the Navy’s top brass.

Study 1: Conducted at the Gallups Island Quarantine Station between Nov 6 - Dec 23, 1918. Total of 68 participants (U.S Navy sailors). 0/68 became ill.

Study 2: Conducted at the Angel Island Quarantine Station between Nov 6 - Dec 23, 1918. Total of 50 participants (U.S Navy sailors). 0/50 became ill.

Study 3: Conducted at the Gallups Island Quarantine Station between February 4 and March 10, 1919. Total of 49 participants (U.S Navy sailors). 0/49 became ill.

The experiments involved men being inoculated with the flu virus. They breathed in germs from jars, they had mucous from infected people syringed in to their eyes, mouths, throats and nasal passages. They drank infected mucous. They had infected men breathe and cough in to their open mouths (almost mouth to mouth). They had infected peoples mucous injected in to their veins. They spent time in hospital wards with infected people talking, shaking hands and even sleeping in the same beds as them. None of the 167 healthy participants fell sick. Here we have three separate studies, conducted by different medical teams, with different participants, at different times and places, yet they all came to the same conclusion. Despite their attempts, they were never able to prove that the Spanish Flu was contagious.   

Could Fear Cause Disease?

Whilst gathering research for this blog, I came across a fantastic newspaper article published in the Glendale Evening News and the Oakland Enquirer on February the 6th, 1919. The article titled an “Official Test” reported on the results of the U.S Navy studies (quote)25; “The experiments made at Goat Island by Navy doctors in an effort to learn something about the influenza germ, carry a lesson that every person should study an understand.

Fifty young sailors volunteered to become influenza victims that the doctors might study the disease more carefully. These young men had no fear of the disease; they willingly offered themselves. They were placed with flu patients; they were given jars of flu germs which they breathed into their lungs; they had flu germs injected in to their bodies. Then the medical men prepared to study the cases as they developed. But no cases developed among these fifty sailors!

These men had been inoculated; they had been exposed to the disease in every manner; they had breathed in the germs and eaten and slept with flu victims and not one of them became infected. The medical men confessed themselves baffled. All their ideas of the disease were turned topsy-turvy. The bunk about the masks was again exposed; and it was shown that the disease was not communicable, not contagious. The doctors are still wondering. The explanation however is simplicity itself, for it was proved by each of these fifty young men.

These fifty young men volunteered to act as subjects upon which to be experimented. This showed clearly that they did not fear the disease. In other words, they could not acquire what they did not fear. Since their fear of the disease was gone, the disease was absolutely non-existent, even though every effort was made to force it on them.

There can be no clearer nor better proof of the oft stated and rapidly being accepted fact that mind controls matter. Medical men are now acknowledging this condition. They are the first to tell patients to eliminate fear. When this is done, their work is done. There would be no cases of influenza if every person in the State would do as these fifty Goat Island sailors did; namely eliminate fear of the disease”.

Tales of Conjoined Twins

In my attempt to understand if germs do in fact cause disease, I wondered if there was any documented evidence about communicable diseases in conjoined twins. Given that conjoined twins are always in close proximity to one another and are exposed almost the exact same environmental conditions, one could assume that they would fall ill at the same time when exposed to infectious diseases. I was able to locate a number of cases where one twin fell ill with an infectious disease, whilst the other remained completely healthy.

Radica and Doodica Khettronaik (known as the Orissa twins) were conjoined twins born on September 1889, in the Indian province of Orissa26. In 1902 at the age of 13, when Doodica contracted tuberculosis, a medical doctor by the name of Professor Doyen attempted to separate them. Unfortunately, Doodica died, however her sister Radica remained completely healthy and survived. Tuberculosis is considered to be a highly infectious and potentially lethal disease affecting the respiratory system, caused by Mycobacterium tuberculosis27,28. How is it possible that only one twin contracted this highly infectious disease, despite being in such close proximity to one another?

Then there is the case of the conjoined twins Masha and Dasha Krivoshlyapova, born in Russia in 1950. The sisters shared an interconnected blood supply and immune system, however they had  separate central nervous systems29. Despite sharing an immune system, the twins reacted to illness completely differently. Dasha was prone to colds and had measles during her childhood, whilst her sister Masha, remained completely healthy30.

Finally, there is the story of the conjoined twins Rosa and Josepha Blazek who were born in 1878. Just like Masha and Dasha, Rosa and Josepha had an interconnected blood supply and immune system, but had a separate central nervous system. In February of 1922, Rosa first became ill with a cough, which then developed in to influenza, whilst Josepha remained unaffected. Three weeks later, Rosa had convalesced, however within days, Josepha experienced severe abdominal pain and jaundice, which was diagnosed as cholecystitis. The sisters were hospitalised but later died31.

How is it that influenza or tuberculosis was not spread to the other twin, given they were in such close and constant proximity to each other? Also why didn’t the original infection infect both of them? Is it possible that they were both exposed to similar environmental factors or toxins, yet their diseases manifested in different ways? In these cases, the twins shared a blood supply and immune system, but had separate nervous systems. Therefore, could the nervous system may play a more significant role in the development of illness than we currently understand?

What Really Makes Us Sick?

Let’s assume for a moment that terrain theory is indeed the correct theory. This would mean that there are no pathogenic infectious microorganisms that cause disease. So what really makes us sick, and what are the alternative explanations that could account for “infectious disease”? We certainly do not claim to have all of the answers, nor do we know precisely what causes so called infectious disease in humans. Despite all of the wonders of modern science, there are many things that we may never know the answer to. For example, how do birds or fish know when to turn in perfect unison when flying in a flock or school? How do dogs known when their owners are coming home32,33?

Many women will report that when they live together, after a certain amount of time, their menstrual cycles will synchronise. This phenomenon is known as menstrual synchrony and has been demonstrated in several studies34–36. Whilst a number of theories explaining how this occurs have been proposed in the literature, including social interaction36 and pheromones37, the true cause is unknown. It is unlikely that menstrual synchrony is caused by an infectious agent like a virus, so what is the force that allows human bodies to silently communicate with one another in such a way? Is this the same force that causes people to become sick at the same time?

Alimuddin Zumla, who is a Professor of Infectious Disease at University College of London, has published a number of papers discussing the role of the terrain in disease. In a 2011 paper38, he mentions that “A large proportion of pulmonary infections seen in medical practice today predominantly occur due to disturbances in the ‘terrain’. Many of these are elegantly described in the articles written by experts in their fields in this issue of Current Opinion in Pulmonary Medicine. Claude Bernard and his colleagues were ‘spot on’ in proposing the pleomorphic theory for infectious diseases, and the theory still holds true today over a century later”. In another paper published by Professor Zumla in 2011, he concluded that the high prevalence of disease in prisoners is due to a range of factors that compromise the terrain. Such factors include poor nutrition, smoking, drugs, loss of dignity, liberty, autonomy and privacy, inadequate accommodation and poor health care39. In a 2015 paper, he proposed that therapies targeting the terrain should be explored in the treatment of multi-drug resistant tuberculosis40.

Terrain theory proposes that illness arises from within us, meaning that there is some type of insult, which disrupts our internal environment and cellular homeostasis. This could be from many factors including poor nutrition, smoking, drugs, loss of dignity etc as mentioned by Professor Zumla39. When the internal environment is disrupted, or when cells become nutrient depleted, poisoned or toxic, the body may initiate a self-repair process that stimulates detoxification and tissue regeneration. We could think of a cold or flu as a kind of “spring clean” for our body. At first, this may seem non-sensical, however the literature contains many instances of people experiencing flu like symptoms after being exposed to toxins and poisons.  

In a recent Humanely podcast, Dr. Robert Young provided an in-depth overview of several causes of disease according to the Terrain theory model. He mentions that one of the main causes of disease is from changes to the pH of the terrain (which is the interstitial fluid). We encourage you to listen to that podcast here

Are Toxins and Poisons to Blame?

The word virus originated from the Latin word meaning “poison” or “venom”41. In part I, we introduced the topic of exosomes, which are microscopic particles that are basically identical to viruses. In fact, exosomes are so similar to viruses that they have been referred to as “a virus in every sense of the word”42. Exosomes are thought to be produced by cells for cellular communication purposes43. Interestingly, cells also produce exosomes is in response to environmental toxins and poisons44 and have been likened to garbage bags full of waste products45,46. When a cell gets poisoned or overburdened with metabolic waste products, it packs the waste in to an exosome and expels it in to the extracellular space45,46. Have viruses just been mistaken for exosomes?  

There are many instances of exposure to toxins and poisons causing flu like symptoms in the literature. Let’s take Metal Fume Fever for example, which is also known as ‘galvanisers poisoning’, ‘smelters chills’, or ‘Monday morning fever’47. Within 48 hours of being exposed to fumes containing heavy metals, an affected individual can become ill with an influenza like illness. The symptoms of Metal Fume Fever are so similar to that of the flu (fever, chills, myalgia, chest pain, non-productive cough, headache and malaise), an article published in the Australian Family Physician warned clinicians to conduct a thorough clinical examination and occupational history check to be able to ensure that misdiagnosis is avoided. Interestingly, the symptoms of Metal Fume Fever begin to subside after 48 hours47 but can last up to five days48, a very similar duration to that of the flu. It is also well established that acute pesticide exposure causes flu like illness 49,50. For example, sheep farmers often suffer from an illness known as Dippers Flu which occurs within 24 hours after treating sheep with pesticides. Symptoms of Dippers Flu can last up to 7 days and include headache, myalgia, malaise, runny nose, muscle weakness, fever, dizziness and coryza50.

From this evidence, we can deduce that acute toxin and poison exposure can cause symptoms that are very similar to that of the common cold or flu. We can also deduce that the symptoms associated with the common cold or flu may occur as a ‘self cleaning mechanism’ in attempt to detoxify the body from toxins. Is It reasonable to assume, that if we are exposed to various toxins and poisons over a prolonged period (let’s say 12 months), that our body might undergo a similar detoxification process observed in metal workers and sheep farmers?

According to the terrain theory, when a cell becomes sick, toxic, poisoned, nutrient depleted or damaged, bacteria arise from microzyma that are able to target and break down a specific type of poison or damaged tissue. It is postulated that the bacteria obeserved in the presence of disease are not the cause, but rather the result of disrupted homeostasis. 

But what might explain the seasonal nature of infections like the flu? Toxic and carcinogenic substances known as polycyclic aromatic hydrocarbons are present in the highest atmospheric concentrations in the Winter months and are lowest in the summer months51. Aromatic polycyclic hydrocarbons have also been found in very high concentrations in snow. As the snow falls through the atmosphere it absorbs these toxins, which is one reason why the air seems so crisp after snow fall. As the snow melts towards the end of Winter, these toxins are released in to the and are considered to be a considerable hazard to human health52. Is it possible that colds and flu’s are a detoxification response due to the heightened seasonal exposure to environmental toxins in the Winter months?

Concluding Remarks

If infectious agents are the cause of disease, why are approximately 50% influenza cases53, 95% of polio cases54, 96% of corona-virus cases55, and more than 90% of hepatitis C cases asymptomatic56? If a germ really does cause disease, then why do so many "infected" people never become ill? Why can people have a Streptococcus throat infection, yet have no symptoms57? How can up to 50% of people with a urinary tract infection (bacteriuria) be asymptomatic58? Why do 95% of people with Mycobacterium tuberculosis infections never show signs or symptoms of the disease59?

If infectious agents truly do cause disease, where are the randomized controlled clinical trials that prove unequivocally, that viruses and bacteria do indeed cause disease? There is no doubt that these are difficult to undertake given ethical considerations.

Make sure to stay tuned for part III of “What Really Makes Us Sick? The Terrain or the Germ?”, which will discuss some practical measures that we can take to strengthen the terrain of the body and reduce our risk of illness.

Note: This article is for general information purposes only. It does not constitute as health advice and does not take the place of consulting with your primary health care practitioner. 

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References

  1. Hume E. Béchamp or Pasteur? A Lost Chapter in the History of Biology. 1923.
  2. O Young R. Second Thoughts about Viruses, Vaccines, and the HIV/AIDS Hypothesis - Part 1. Int J Vaccines Vaccin. 2016;2(3). doi:10.15406/ijvv.2016.02.00032
  3. Haschek WM, Rousseaux CG, Wallig MA. Manifestations of Toxic Cell Injury. In: Fundamentals of Toxicologic Pathology. Elsevier; 2010:9-42. doi:10.1016/B978-0-12-370469-6.00002-7
  4. Logan DC. The mitochondrial compartment. J Exp Bot. 2006;57(6):1225-1243. doi:10.1093/jxb/erj151
  5. Joshi HM, Toleti RS. Nutrition induced pleomorphism and budding mode of reproduction in Deinococcus radiodurans. BMC Res Notes. 2009;2(1):123. doi:10.1186/1756-0500-2-123
  6. Doolittle WF. Microbial neopleomorphism. Biol Philos. 2013;28(2):351-378. doi:10.1007/s10539-012-9358-7
  7. Enderlein E. Bacteria Cyclogeny. Prescott: Enderlein Enterprises Inc; 1925.
  8. Martel J, Wu C-Y, Huang P-R, Cheng W-Y, Young JD. Pleomorphic bacteria-like structures in human blood represent non-living membrane vesicles and protein particles. Sci Rep. 2017;7(1):10650. doi:10.1038/s41598-017-10479-8
  9. Pleomorphic Bacteria. Lancet. 1933;222(5755):1384-1385. doi:10.1016/S0140-6736(00)90835-3
  10. Bird C. The Persecution and Trial of Gaston Naessans. Tiburon: H.J Kramer Inc; 1991.
  11. Odeh M. Sepsis, septicaemia, sepsis syndrome, and septic shock: the correct definition and use. Postgrad Med J. 1996;72(844):66. doi:10.1136/pgmj.72.844.66
  12. Villequez E. L’étude biochimique du sang ne doit pas méconnaître le rôle des évolutions de corpuscules existant dans ce milieu. In: ; :752-755. doi:10.1159/000384343
  13. TEDESCHI GG, AMICI D, PAPARELLI M. Incorporation of Nucleosides and Amino-acids in Human Erythrocyte Suspensions: Possible Relation with a Diffuse Infection of Mycoplasms or Bacteria in the L Form. Nature. 1969;222(5200):1285-1286. doi:10.1038/2221285a0
  14. Tedeschi GG, Amici D, Paparelli M. The uptake of radioactivity of thymidine, uridine, formate, glycine and lysine into cultures of blood of normal human subjects. Relationships with mycoplasma infection. Haematologia (Budap). 1970;4(1):27-47. http://www.ncbi.nlm.nih.gov/pubmed/5522357.
  15. Tedeschi GG, Amici D. Mycoplasma-like microorganisms probably related to L forms of bacteria in the blood of healthy persons. Cultural, morphological and histochemical data. Ann Sclavo. 1972;14(4):430-442. http://www.ncbi.nlm.nih.gov/pubmed/4130434.
  16. PEASE PE. Tolerated Infection with the Sub-bacterial Phase of Listeria. Nature. 1967;215(5104):936-938. doi:10.1038/215936a0
  17. Pease PE, Bartlett R, Farr M. Incorporation of14C-thymidine by cultures of erythrocytes from rheumatoid arthritis patients and normal subjects, suggesting the presence of an L-form. Experientia. 1981;37(5):513-515. doi:10.1007/BF01986169
  18. Pease PE, Tallack JE. A permanent endoparasite of man. 1. The silent zoogleal/symplasm/L-form phase. Microbios. 1990;64(260-261):173-180. http://www.ncbi.nlm.nih.gov/pubmed/2084495.
  19. Wu W, Wei L, Feng Y, Kang M, Zong Z. Enterobacter huaxiensis sp. nov. and Enterobacter chuandaensis sp. nov., recovered from human blood. Int J Syst Evol Microbiol. 2019;69(3):708-714. doi:10.1099/ijsem.0.003207
  20. Bartlett R, Bisset KA. Induction of Reversion From the L-Form to the Sporogenous Phase of Bacillus Licheniformis Var. Endoparasiticus (Benedek). J Med Microbiol. 1979;12(2):239-244. doi:10.1099/00222615-12-2-239
  21. Mattman L. Cell Wall Deficient Forms: Stealth Pathogens. 3rd ed. CRC Press; 2000.
  22. Castillo DJ, Rifkin RF, Cowan DA, Potgieter M. The Healthy Human Blood Microbiome: Fact or Fiction? Front Cell Infect Microbiol. 2019;9. doi:10.3389/fcimb.2019.00148
  23. McLaughlin RW, Vali H, Lau PCK, et al. Are there naturally occurring pleomorphic bacteria in the blood of healthy humans? J Clin Microbiol. 2002;40(12):4771-4775. doi:10.1128/jcm.40.12.4771-4775.2002
  24. Rosenau MJ. Experiments to determine mode of spread of influenza. J Am Med Assoc. 1919;73(5):311-313. doi:10.1001/jama.1919.02610310005002
  25. An Official Test. Glendale Evening News. https://archive.org/details/cgl_003686/page/n3/mode/2up. Published 1919.
  26. Windle B. Report on Recent Teratological Literature. J Anat Physiol. 1895;29:463-470.
  27. Luzzati R, Migliori GB, Zignol M, et al. Children under 5 years are at risk for tuberculosis after occasional contact with highly contagious patients: outbreak from a smear-positive healthcare worker. Eur Respir J. 2017;50(5):1701414. doi:10.1183/13993003.01414-2017
  28. Abarca Tomás B, Pell C, Bueno Cavanillas A, Guillén Solvas J, Pool R, Roura M. Tuberculosis in Migrant Populations. A Systematic Review of the Qualitative Literature. Goletti D, ed. PLoS One. 2013;8(12):e82440. doi:10.1371/journal.pone.0082440
  29. Craig JM. A twin tale to keep you up at night. Science (80- ). 2017;357(6352):653-653. doi:10.1126/science.aao1869
  30. Quigley C. Conjoined Twins: An Historical, Biological and Ethical Issues Encyclopedia. Nort Carolina: McFarland & Company; 2003.
  31. Kokcu A, Cetinkaya MB, Aydin O, Tosun M. Conjoined twins: Historical perspective and report of a case. J Matern Neonatal Med. 2007;20(4):349-356. doi:10.1080/14767050701228438
  32. Sheldrake R. A Dog That Seems to Know When His Owner Is Coming Home: Videotaped Experiments and Observations. J Sci Explor. 2000;14(2):233-255.
  33. Taylor R. Dogs That Know When Their Owners Are Coming Home: And Other Unexplained Powers of Animals. J Parapsychol. 2001;65(1):90-96.
  34. Morofushi M. Positive Relationship between Menstrual Synchrony and Ability to Smell 5alpha-Androst-16-en-3alpha-ol. Chem Senses. 2000;25(4):407-411. doi:10.1093/chemse/25.4.407
  35. Graham CA. Menstrual synchrony. Hum Nat. 1991;2(4):293-311. doi:10.1007/BF02692195
  36. MCCLINTOCK MK. Menstrual Synchrony and Suppression. Nature. 1971;229(5282):244-245. doi:10.1038/229244a0
  37. Pettit M, Vigor J. Pheromones, feminism and the many lives of menstrual synchrony. Biosocieties. 2015;10(3):271-294. doi:10.1057/biosoc.2014.28
  38. Zumla A. Pulmonary infections: ‘le terrain est tout, le microbe n’est rien.’ Curr Opin Pulm Med. 2011;17(3):131-133. doi:10.1097/MCP.0b013e328345873a
  39. O’Grady J, Mwaba P, Zumla A. The health of prisoners. Lancet. 2011;377(9782):2001. doi:10.1016/S0140-6736(11)60857-X
  40. Zumla A, Maeurer M. Host-Directed Therapies for Tackling Multi-Drug Resistant Tuberculosis: Learning From the Pasteur-Bechamp Debates: Table 1. Clin Infect Dis. 2015;61(9):1432-1438. doi:10.1093/cid/civ631
  41. Zimmer B. Virus: The Spread of a Latin Term for Poison. Wall Street Journal. https://www.wsj.com/articles/virus-the-spread-of-a-latin-term-for-poison-11582305835. Published 2020.
  42. Wells WA. When is a virus an exosome? J Cell Biol. 2003;162(6):960-960. doi:10.1083/jcb1626rr1
  43. Maia J, Caja S, Strano Moraes MC, Couto N, Costa-Silva B. Exosome-Based Cell-Cell Communication in the Tumor Microenvironment. Front Cell Dev Biol. 2018;6. doi:10.3389/fcell.2018.00018
  44. Harischandra DS, Ghaisas S, Rokad D, Kanthasamy AG. Exosomes in Toxicology: Relevance to Chemical Exposure and Pathogenesis of Environmentally Linked Diseases. Toxicol Sci. 2017;158(1):3-13. doi:10.1093/toxsci/kfx074
  45. H. Rashed M, Bayraktar E, K. Helal G, et al. Exosomes: From Garbage Bins to Promising Therapeutic Targets. Int J Mol Sci. 2017;18(3):538. doi:10.3390/ijms18030538
  46. Vidal M. Exosomes: Revisiting their role as “garbage bags.” Traffic. 2019;20(11):815-828. doi:10.1111/tra.12687
  47. Wong A, Greene S, Robinson J. Metal Fume Fever. Aust Fam Physician. 2012;41(3):141-143.
  48. Cain JR, Fletcher RM. Diagnosing metal fume fever--an integrated approach. Occup Med (Chic Ill). 2010;60(5):398-400. doi:10.1093/occmed/kqq036
  49. Solomon C, Poole J, Palmer KT, Peveler R, Coggon D. Acute symptoms following work with pesticides. Occup Med (Chic Ill). 2007;57(7):505-511. doi:10.1093/occmed/kqm066
  50. Povey AC, Rees HG, Thompson JP, Watkins G, Stocks SJ, Karalliedde L. Acute ill-health in sheep farmers following use of pesticides. Occup Med (Chic Ill). 2012;62(7):541-548. doi:10.1093/occmed/kqs099
  51. Liu D, Xu Y, Chaemfa C, et al. Concentrations, seasonal variations, and outflow of atmospheric polycyclic aromatic hydrocarbons (PAHs) at Ningbo site, Eastern China. Atmos Pollut Res. 2014;5(2):203-209. doi:10.5094/APR.2014.025
  52. Nazarenko Y, Fournier S, Kurien U, et al. Role of snow in the fate of gaseous and particulate exhaust pollutants from gasoline-powered vehicles. Environ Pollut. 2017;223:665-675. doi:10.1016/j.envpol.2017.01.082
  53. Weinstein R, Bridges C, Kuehnert M, Hall C. Transmission of Influenza: Implications for Control in Health Care Settings. Clin Infect Dis. 2006;42(5):737-737. doi:10.1086/500947
  54. Groce NE, Banks LM, Stein MA. Surviving polio in a post-polio world. Soc Sci Med. 2014;107:171-178. doi:10.1016/j.socscimed.2014.02.024
  55. COVID-19 in Correctional and Detention Facilities — United States, February–April 2020. Centers Dis Control Prev. 2020;69(19):587-590.
  56. Hepatitis C. Victoria Health. https://www2.health.vic.gov.au/public-health/infectious-diseases/disease-information-advice/hepatitis-c. Published 2020. Accessed October 25, 2020.
  57. Martin J. The Streptococcus Pyogenes Carrier State.; 2016. http://www.ncbi.nlm.nih.gov/pubmed/27466665.
  58. Givler DN, Givler A. Asymptomatic Bacteriuria.; 2020. http://www.ncbi.nlm.nih.gov/pubmed/28722878.
  59. Jilani TN, Avula A, Zafar Gondal A, Siddiqui AH. Active Tuberculosis.; 2020. http://www.ncbi.nlm.nih.gov/pubmed/30020618.
  60. Vancová M, Rudenko N, Vaněček J, et al. Pleomorphism and Viability of the Lyme Disease Pathogen Borrelia burgdorferi Exposed to Physiological Stress Conditions: A Correlative Cryo-Fluorescence and Cryo-Scanning Electron Microscopy Study. Front Microbiol. 2017;8. doi:10.3389/fmicb.2017.00596
  61. Robertson P, Abdelhady H, Garduno RA. The many forms of a pleomorphic bacterial pathogen—the developmental network of Legionella pneumophila. Front Microbiol. 2014;5. doi:10.3389/fmicb.2014.00670
  62. Ayoade MS. Pleomorphism and Germ Terrain Dualism. JOJ Nurs Heal Care. 2018;8(3). doi:10.19080/JOJNHC.2018.08.555738
  63. O Young R. Who Had Their Finger on the Magic of Life - Antoine Bechamp or Louis Pasteur? Int J Vaccines Vaccin. 2016;2(5). doi:10.15406/ijvv.2016.02.00047
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