Candida can only exist as saprophyte Second Non-integer epitheliums (erosions, abrasions, etc.), absence of stage debilitating factors, unusual transitory conditions (acidosis, metabolic disorder, and microbial disorder). Candida expands superficially (classic mycosis, both exogenous and endogenous). Third Non-integer epitheliums, presence of debilitating factors (toxic, stage radiant, traumatic, neuropsychic, etc.).
Candida goes deeper into the sub-epithelial levels from which it can be carried to the whole organism through the blood and lymph (intimate mycosis). (12) Stages one and two are the most studied and known, while stage three, though it has been described in its morphological diversity, is reduced to a silent form of saprophytism.
This is not acceptable from a logical point of view, because no one can demonstrate the harmlessness of the fungal cells in the deepest parts of the organism. In fact, the assumption that Candida can behave in the same saprophytic manner that is observed on integer epitheliums when it has successfully penetrated the lower levels is at least risky, because the assumption would have to be sustained by concepts that aretotally aleatory.
In fact, we asked not only to accept a priori that the connective environment is
(a) not suitable to nourish the Candida, but also at the same time to accept
(b) the omnipotence of the body’s defence system towards an organic structure that is invasive but that then becomes vulnerable once lodged in the deeper tissues.
As to point a), it is difficult to imagine that a micro-organism so able to adapt itself to any sub-strata cannot find elements to support itself in the human organic substance; by the same token, it seems risky to hypothesise that the human organism’s defence system is totally efficient at every moment of its existence.
Finally, the assumption that there is a tendency to a state of quiescence and vulnerability in the case of a pathogenic agent such as fungus — the most invasive and aggressive microorganism existing in nature — seems to carry a whiff of irresponsible.
It is therefore urgent, on the basis of the above-mentioned considerations, to recognise the hazardous nature of such a pathogenic agent, which is capable of easily taking the most various biological configurations, both biochemical and structural, in function of the condition of the host organism.
The fungal expansion gradient in fact becomes steeper as the tissue that is the host of the mycotic invasion becomes less eutrophic, and thus less reactive.
To that end, it seems useful to briefly consider the “benign tumour” nosological entity. This is an issue that always appears in general pathology but that indeed is brushed aside most of the time too easily, and it is overlooked, since it usually doesn’t create either problems or worries. It constitutes one of those underestimated grey areas seldom subjected to rational, fresh consideration.
If the benign tumour, however, is not considered a full-fledged tumour, it would be advantageous, for clarity, to categorise it in an appropriate nosological scheme. If, instead, it is thought that it fully belongs to neoplastic pathology, then it is necessary to consider its non-invasive character and consequently to consider the reasons for this.
It is in fact evident how in this second scenario, the thesis based on a presumed predisposition of the organism to auto-phagocytosis, having to admit an expressive graduation, would stumble into such additional difficulties such as to become extremely improbable.
By contrast, in the fungal scenario, the mystery of why there are benign and malignant tumours is exhaustively solved, since they can be recognised as having same etiological genesis.