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Research ArticleOpen Access

Human Cells May Transform Two Microorganisms and Cause Infections Volume 4 - Issue 4

Alen J Salerian*

  • Institution Modern psychiatry, Greece

Received: May 11, 2018;   Published:May 16, 2018

*Corresponding author: Alen J Salerian, Institution Modern psychiatry, ZAIMI 8, Paleo Falero, 17562, Athens Greece, Tel: 306983723947; Email:

DOI: 10.26717/BJSTR.2018.04.001080

Abstract PDF


This study provides scientific evidence to suggest that human cells may transform to microorganisms and represent an independent source of some infections. Evidence consistent with the 99.9% probability of this hypotheses to be correct is presented.Two questions ”Do 38 trillion microorganisms that live in human bodyalways come from outside ?” and “ Do host cellshave the essentials totransform to microorganisms ?” prompt a reviewof genetic, epidemiological , biological and clinicalobservationsin support of thecentral hypotheses.The followingtenobservations are of essence

a) Host cells do have the essentials to produce microorganisms.

b) Human cells transform to other cells such as cancer and stem cells.

c) Rare scavenger microorganisms unelated to normal flora are crucial in corpse decomposition.

d) Opportunistic infections by microorganisms of higher geneticcomplexity emerge upon severeinjuries causingmassivecellular regeneration and death.

e) Aspergillus fumigatus grow in abundancein organic matter such as decaying leaves. andin the outdoor air oflarge scale compostingof sewagesludge factories.

f) Pseudomonasaeruginosaa common cause of opportunistic infections -have larger genome size and higher genetic complexity. g) Genetic influences play an important role in some infections in immunocompetenthosts.

g) Genetic influences play an important role in some infections in immunocompetenthosts.

h) Some infections emerge without host to host transmission.

i) Extraordinary stress from diverse origins may trigger transformation of human cells to microorganisms consistent with the proven link between diverse infections, disorders and changes in host bacterial community.

j) Most reactions on earth are bi-directional. The Implication of theobservation that human cells may transform to bacteria or fungusare:

i. Some infections may be caused by human cells transforming to microorganisms.

ii. Some opportunistic and nosocomial infections may represent transformation of human cells to virulent microorganisms.

iii. Prevention and treatment of infections should address possible transformation of bacteria from human cells.

iv. Experimental validation of the central hypotheses is necessaryandmight bedemonstrated by experimental transformation of stressed or dying human cells to microorganisms.

Keywords: Bacteria, Transformation, Infection


The numbers of bacteria that live in human body are estimated to be 38 trillion with their projected weight of 200 g [1]. Microorganisms play an important role in maintaining normal human function and can also cause infections in complex multicellular organisms. In 1880 Pasteur demonstrated exposure to microorganisms was necessary for fermentation and infections. Since then the germ theory has become a central paradigm for medicine [2]. A recent hypotheses suggested pathways independent of exposure to microorganisms from human cells may produce infections, suggested that exposure and transformation are not mutually exclusive andthus exposure tomicroorganismsby itselfcannotinvalidate independent pathways of bacterial or fungal growth [3].

Consistent with the germ theory, the current medical guidelines to prevent and treat infectious disorders presume that all infections originate from microorganisms invading a human host or a complex multi cellular organism.For instance hospital infections often caused by relatively rare microorganisms such as pseudomonas aeroginisa or aspergillus fumigatus are presumed to be associated with less than perfectsterile conditions of medical equipment or hospital environment. In general our traditional medical understanding and treatment of infectious disorders seem tobe scientifically sound and well proven. However is it possible that some infections may have origins independent of existing microorganisms? Is it possible for some infections to originate from the transformation of human cells to bacteria or fungus under special conditions?

A simple reason to consider an independent pathway for bacterial or fungal infections is because traditional medical understanding and treatment of infectious disorders based upon the germ theory seems to clash with our knowledge of the origin of life on earth. Earth sciences suggest the earth was lifeless for billions of years before the arrival of bacteria and other unicellular organisms.Over a long period of time unicellular organisms have evolved into complex multi cellular organisms including human beings.In essence we know that, microorganisms may originate from nonliving things andthey do not always have to be generated from existing microorganisms. Diverse observations suggest bacteria may grow in sterile environments without exposure, first bacteria [4], bacteria discovered in remote regions below the earth surface) [5].

Evidence Consistent with Human Cells may Transform to Microorganisms and Cause Infections

This hypothesis prompts two questions.

A. Can host cells transform to other living cells?

B. Do host cells have the properties to generate microorganisms that created the first bacteria on earth?

i. Unicellular organisms may transform to other living cells (human cells transform to cancer cellsor stem cells transform to specialized cells [6]. Transformation of streptococcusto pneumococcus [7] and between pneumococcusand three strains of streptococci have been demonstrated [8]. Also a stable leu2- yeast strain has been transformed to LEU2+ by using a chimeric ColE1 plasmid carrying the yeast leu2 gene [9]. Also shown are: transformation of Salmonella typhimurium by plasmid deoxyribonucleic acid [10], Escherichia coli cells undergo plasmid transfection [11]. Naturally competent bacteria are able to undergo genetic transformation [12].

ii. Human cells contain the necessary ingredients –water, carbon, oxygen and nitrogen-to transform to bacteria. This is how unicellular life began on earth 3.5 billion years ago [4]. Also, human cells produce energy (fermentation) [13].

By now, we have proven that human cells contain the properties to generate microorganisms and they are capable to transform to bacteria or fungus. The following genetic, epidemiological, biological and clinicalobservations are ofessence and provide support for theinternal production of microorganismsand not due toexposure or external origin.

A. Normal Flora and the Ubiquitous Presence of Bacteria: Normal flora and the ubiquitous presence of bacteria in soil and in extremely isolated places may suggest that the initial conditions that let microorganisms and bacteria grow from earth may still generate bacteria anywhere [5].

B. Stress of Diverse Aetiology may Alter Host Biology: Is it possible for stress of diverse causation to trigger intracellular changes to transform host cells to microorganisms?.Host bacterial community plays a significant role in protecting host against diverse disorders and infections.Diverse disordersincluding obesity [14], gum disease [15], chronic obstructive pulmonary disease[16], cystic fibrosis[17], asthma [18] colitis and arthritis [19]seem to be mediated by the type and density of bacterial communities in the gut, oral cavity, lungs, lungs, lungs and, gut, gut and joints respectively.

Significant alterations of host bacterial community and also penetrating injuries, burns, massive tissue loss, generalized wasting- maybe stressful for human cells..These observations are consistent with Acinetobacter spp [19] Pseudomonas aeruginosa [20-22] infections in hosts with significant thermal or suninduced tissue losses.

C. Dying host cells seem to be a prerequisite for opportunistic infections (caused by rare microorganismsup (Table 1). Massive cellular death and degeneration almost always pre or co-exist with opportunistic infections.Rare microorganismscause infections in immunocompetent victimsupon severeinjurieswith massivecellular regeneration and death [19-22]. Rarity of causalmicroorganismsandabundance of essential elementsare consistent with cellular transformation.

Table 1:Cycle of Earth Living cells and non-living things transform to living cells and non-living things.

D. Emergenceof rarescavenger microbes during mammalian corpse decomposition. Death of a large and complex multicellular organism creates a giant factory of microorganisms that convert proteins and lipids into foul smelling compounds such as cadaverine , putrescine and ammonia. Studies of mice are, swine and human corpses indicate that microbial communities change significantly during decomposition [23]. Studies are also consistent with the observation that the microbial decomposer community may emerge from multiple environments in which decomposer- scavenger organisms are often rare before decomposition begins [23]. The spectacularmicrobialovergrowth and their low abundance in natureseem to be paradoxicaland consistentwith the central hypotheses . Furthermore the exact origin ofmicrobial decomposer communityis unknown.

E. Abundant presence of aspergillus fumigatusinorganic matter.Aspergillus fumigatus,opportunisticmicroorganisms are abundantin organic matter such as decaying leaves., compost heaps, silos ,grain storage beans andin the outdoor air oflarge scale composting of sewage sludge factories [24].

F. Pseudomonas aeruginosa is one of the three causes of opportunistic infections and meningitis have higher evolutionary architecture [25] (Tables 2-5) consistent with the following properties: Greater genetic complexity. Greater genome size and functional complexity.For rare bacteria to be one of the 3mostcommon causes ofopportunistic infectionsis an obvious paradox. The statistical likelihood of this infection being importedis relatively low. This observation, along withthehigher geneticcomplexity of Pseudomonas aeruginosa significantly increases the likelihood thatthe abundance of essential substances at a timeof tissue death and degenerationmight have contributed to the infection.

Table 2:Living cells transform to other living cells.

Table 3:Cellular Death And Opportunistic Infections.

Table 4:Cellular Death, Alteration In Host Bacterial Community and Various Disorders.

Table 5:Pseudomonas Aeruginosa: Internal or External Production.

G. Genetic susceptibility of immunocompetent hosts to develop tineaversicolor infections [26]. Noteworthy are, clinical observations to suggest no host to host transmission.


Consistent withtheobservations that host cells can transform to other living cells,contain the properties ofearth thatgenerated the first bacteriaand consistent with the bidirectional nature of life and diverse observations of possible microbial transformation from stressedor dying host cells, we canstate thatcells ofcomplex multicellular organisms may transform to bacteria. Two weaknesses of this thesis are evident:

a) Specific pathways of transformation from animal cells to bacteria are unknown.

b) Absence of experimental validation.

Despite its weaknesses, the probability of” host cells ofcomplex multicellular organisms may transform to microorganisms is extremely high. Experimental validation is the next logical step. Experimental transformation of stressed or dying human cells to microorganismsseems to be a reasonable strategy.


Some infections may be caused by transformation of human cells to microorganisms. Some opportunistic and nosocomial Infections may represent transformation of human cells to virulent microorganisms. Prevention and treatment of infections should also address possible transformation of bacteria from human cells.


I am grateful to Nansen G SaleriPhD, James H Fetzer PhD and Fredrik Karlsson for their helpful input.


  1. Sender R, Fuchs S, Milo R (2016) Revised estimates for the number of human and bacteria cells in the body. PLoS Biol 14(8): e10R
  2. Pasteur L (1880)And the extension of the germ theory to the aetiology of certain common diseases. Comptesrendusdel’Academie des Sciences. xc.Ernst,(Ttrans) 188:1033-44.H.C.
  3. Salerian AJ (2017) Human body may produce bacteria, Medical Hypotheses103: 131-132.
  4. VanHolde KE (1980) The origins of life and evolution.: Allan R Liss, NewYork, USA.
  5. Gorman J (2013) Scientists Find Life in the Cold and Dark Under Antarctic Ice,@nytimesscience.
  6. Krause DS, Thiese ND, Collector ML, et al. (2001) 4Multi-Organ, Multi- Lineage Engraftment by a Single Bone Marrow-Derived Stem Cell, CELL 105: 369-377,
  7. Rosenow EC (1914) Test mutations within the streptococcus enamel proper school . Journal of Infectious Disorders 14(1:1-)32.
  9. Hinnen A, Hicks JB, Fink JR (1978) Transformation of yeast. Proceedings National Academy of Sciences 75: 1929-1933.
  10. Lederberg EM, Cohen SN (1974) Transformation of Salmonella typhimurium by Plasmid Deoxyribonucleic Acid. J Bacteriol 119: 1072- 1074.
  11. Lnoue H, Nojima H, Okayama H (1990) High efficiency transformation of Escherichia coli with plasmids. Gene 96: 23-28.
  12. Chen I, DubnauD (2004) DNA uptake during bacterial transformation, Nature Reviews Microbiology 2: 241-249.
  13. Anaerobic Cellular Respiration (2016) Boundless BIology Textbooks 365-1159, Boundless
  14. Ley RE, Turnbaugh PJ, Klein S, Gordon JS (2006) Microbial ecology:Human gut microbes associated with obesity. Nature 444: 1022-1023.
  15. Kumar PS, Leys EJ , Bryk JM ,Martinez FJ , Moeschberger ML, et al. (2006) Changes in periodontal health status are associated with bacterial community shifts as assessed by quantitative 16 S cloning and sequencing. Journal Clinical Microbiology 44: 3665-3673.
  16. Pragman AA, Kim HB (2012) Reilly CS Wendt C Isaacson RE. The microbiology in moderate and severe chronic obstructive pulmonary disease. PLOS One 7(10):1-10.
  17. Bittar F, Richet H, Dubus JC, Reynaud–Gabert M, Stremier N, et al. (2008) Molecular detection of multiple emerging pathogens in sputa in cystic fibrosis patients. LLoS One 3: e2908.
  18. Hilty M, Burke C, Pedro H (2010) Disordered Microbial communities in asthmatic airways. PLOS One 510: 8578.
  19. Rath HC,Herfarth HH,Ikeda JS,Grenther WB, Hamm TE, BallishJt E, et al. (1996) Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis, and arthritis in HLA-B27/human beta2 microglobulin transgenic rats. J Clin Invest 98(4): 945-953.
  20. Winstanley C, Fothergill JL (2009) The role of quorum sensing in chronic cystic fibrosis Pseudomona aeruginosa infections. Microbiology Letters 290(1): 1.
  21. Almasaudi SA (2016) Acinetobacter nosocomial pathogens: epidemiology and resistant features, Saudi Journal Of Biological Sciences.
  22. Baron S (1996).Baron’s Medical microbiology (4th edn.).Univ.of Texas Medical branch.
  23. Balcht A, Smith R (1994) Pseudomonas aeruginosa:Infections and treatment. Informa Health Care 83-84.
  24. Metcalf JM, Zhenjiang ZX, Weiss S (2016) Microbial community assembly and metabolic function during mammalian corpse decomposition. Science 351: 158-162.
  25. Marsh PB, Milner PD, Kla JM (1979) A guide to the recent literature on Aspergillosis as caused by aspergillus fumigatus frequently found in self-healing organic matter. Mycopathologia 69: 67-81.
  26. Stover CK, Pham XQ, Olson MV (2000)Complete genome sequence of Pseudomonas aeruginosa PAO1, an opportunistic pathogen. Nature 406: 959-964.
  27. Hafez Ma,El-Shamy SB (1985) Genetic Susceptibility in Pityriasisversicolor, Dermatologica 171: 86-88.