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ISSN: 2574 -1241
ISSN: 2574 -1241
Received: August 24, 2018; Published: September 06, 2018;
*Corresponding author: Alen J Salerian MD, Organisation Modern Psychiatry, Zaimi street, paleo falero, Athens 17562, Greece
DOI: 10.26717/BJSTR.2018.08.001701
Background: A plethora of evidence suggest pathways independent of contamination may produce microbial growth and infections. Objective: To prove that pathways independent of contamination may produce burn wound infections.
Methods: We searched the keywords burn wound infections in Google scholar and pub med for articles and their references published in English from 2000 to 2017. We then applied the probability theory to calculate the probability of pathways independent of contamination to produce burn wound infections.
Results: Pathways independent of contamination may produce burn wound infections. The probability of certainty of this observation is 99.9998%.
Conclusion: Pathways independent of contamination may produce burn wound infections.
Scientific observations suggest pathways independent of contamination may produce infections [1,2]. For instance, unicellular organisms (prokaryota) including bacteria transformed from lifeless matter 3.5 billion years ago [3-5]. Murchison meteorite contain organic compounds consistent with the existence of vital substances necessary for life in universe [6] Organic compounds were produced by artificial methods [7].
To prove that pathways independent of contamination may produce burn wound infections.
I searched the keywords burn wound infections in Google scholar and Pub Med for articles and their references published in English from 2000 to 2017. We then applied the probability theory to calculate the probability of pathways independent of contamination to produce burn wound infections.
Microorganisms transform to other microorganisms [8]. Human cells transform to different cells [9,10]. A lifeless protein transforms to an infectious prion [11]. Tinea versicolor is caused by microorganisms that are part of normal flora [12,13]. Any one of the three host properties (genetics, medications, skin conditions) determines whether someone develops tinea versicolor [14,15] and this observation is consistent with a cell mediated model in which transformation can be ascribed.
Also, studies indicate tinea versicolor is not contagious and it's not possible to infect a rabbit or human host with tinea versicolor by inoculating pityrosporum orbiculare or pityrosporum ovale without occlusion [14,15]. Together, these results describe a cell mediated model, in which transformation can be ascribed. H. pylori are part of normal gastric flora and result either from contamination or transformation. Epidemiological studies and clinical observations show no evidence of host to host contamination in h.pylori infections [16]. This observation is also consistent with a cell mediated model in which transformation can be ascribed.
Sterile burn wounds treated vigorously with anti-microbial substances always develop infections by very rare pathogens [17,18]. This suggests a cell mediated model in which transformation can be ascribed. The emphasis here is the same as h.pylori and tinea versicolor that burn infections are also cell mediated diseases consistent with transformation. A plethora of evidence suggest normal flora may come from trans formation of human cells consistent with the observations that the amniotic fluid, placenta, milk of healthy neonates are not sterile [19-22].
The probability of a physically possible observation to be correct exponentially increases by each supporting evidence and can be expressed as an equation: C= 100-1/2n ("C"representing the percent probability of certainty and "n "representing the number of diverse evidence consistent with the observation).
This equation is based upon the premise that each supporting evidence or observation is a hypotheses -a logical inference from observing facts from which consequences may be deduced -with a % 50 chance of being correct and therefore the final outcome would be the same as the probability of random occurrence in flipping a coin. Hence it would be like "heads "coming up a consecutive number "n"of times. For instance, the probability of "heads" coming up 3 consecutive times is 1/23 or 1/8 or 11%, 10 consecutive times is 1/210 or % 0.09.
Of crucial significance, consistent with the framework of flipping a coin, potential flaws of statistical analysis - randomness and bias- have no effect on the accuracy of final outcome. As long as it is fair play without tricks it does not matter who flips the coin.
The probability that burn wound infections may result from transformation of human tissue is % 99.9996:
a) Organic compounds were produced by artificial methods [7].
b) A lifeless protein transforms to an infectious prion [11].
c) Microorganisms transform to other microorganisms [8,9].
d) Human cells transform to different cells [10].
e) Lifeless organic matter of earth transformed to microbes [3].
f) Murchison meteorite contain organic compounds consistent with the existence of vital substances necessary for life in universe [6].
g) Amniotic fluid is not sterile [19-22].
h) Meconium is not sterile [20-22].
i) Human milk is not sterile [20-22].
j) Placenta is not sterile [20-22].
k) Tinea versicolor infections are not contagious [12,13].
l) Inoculation of tinea versicolor pathogens do not cause infections without occlusion [14,15].
m) Epidemiological data suggest H pylori-gastric ulcer infections are not transmitted from host to host [16].
n) Bacteria exist in extraordinarily remote locations on earth [23].
o) Theory of evolution [24].
p) Sterile burn wounds vigorously treated with antibiotics in burn units with excellent infection prevention almost always develop microbial growth and infections [17,18].
q) Sterile burn wounds vigorously treated with antibiotics in burn units with excellent infection often develop infections by Pseudomonas aeruginosa PAO1, an opportunistic pathogen with morphological features (large genome size, greater functional complexity and the younger evolutionary age) very different than normal bacteria [17-19,25].
Although, the precise mechanism and pathways of transformation remain unknown, we can state that pathways independent of contamination may generate burn wound infections and the probability of this observation to be correct is 99.9996%.
This discovery may introduce novel treatments for opportunistic infections especially those associated with burns and major trauma. It may improve our understanding of inflammatory disorders and discovering yet unknown environmental influences (sudden temperature changes, exposure to cold) in the pathogenesis of common or unrecognized infections.
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