world of the fungi part2

11) When a cell gets old or becomes damaged (i.e. by a toxic substance or by a pharmaceutical) many fungi whose intercellular septums are provided with a pore react by implementing of a defence process calledprotoplasmic flux through which they transfer the nucleus and cytoplasm of the damaged cell into a healthy one, thus conserving unaltered all their biological potential.
12) The phenomena regulating the development of hyphal ramification are unknown to date (9). They consist either of a rhythmic development, or in the appearance of sectors which, though they originate from the hyphal system, are self-regulating (10), that is, independent of the regulating action and behaviour of the rest of the colony.
13) Fungi are capable of implementing an infinite number of modifications to their own metabolism in order to overcome the defence mechanism of the host. These modifications are implemented through plasmatic and biochemical actions as well as by a volumetric increase (hypertrophy) and numerical hyperplasy of the cells that have been attacked (11).
14) Fungi are so aggressive as to attack not only plants, animal tissue, food supplies and other fungi, but even protozoa, amoebas and nematodes.

Fungi hunt nematodes, for example, with peculiar hyphal modifications that constitute real mycelial criss-cross, viscose, or ring traps that achieve the immobilisation of the worms, as a precursor their hyphal invasion.

In some cases, the aggressive power of fungi is so great as to allow it, with only a cellular ring made up of three units, to tighten in its grip, capture and kill its prey in a short time notwithstanding the prey’s desperate struggling.
From the short notations above, therefore, it seems fair to dedicate a greater attention to the world of fungi, especially considering the fact that biologists and microbiologists constantly highlight large deficiencies and voids in all their descriptions and interpretations of the fungi’s shape, physiology and reproduction.
So the fungus, which is the most powerful and the most organised micro-organism known, seems to be an extremely logical candidate as a cause of neoplastic proliferation. Imperfect Fungi (so called because of the lack of knowledge and understanding of their biological processes) deserve particular attention since their essential prerogative sits in their fermentative capacity.
The greatest disease of mankind may therefore hide within the small cluster of pathogenic fungi, and may be after all be located with just some simple deductions able to close the circle and providing the solution.

Considering that, among the human parasite species, the Dermatophytes and Sporotrichum demonstrate an excessively specific morbidity, and that experience shows that Actinomycetes, Toluropsis and Hystoplasma rarely enter the context of pathology, the Candid Albicans clearly emerges as the sole candidate for tumoral proliferation.
If we stop for a second and reflect on its characteristics, we can observe many analogies with neoplastic disease. The most evident are:

  1. Ubiquitous attachment: no organ or tissue is spared
  2. The constant absence of hyperpyrexia
  3. Sporadic and indirect involvement of the differential tissues
  4. Invasiveness that is almost exclusively of the focal type
  5. Progressive debilitation
  6. Refractivity to any type of treatment
  7. Proliferation facilitated by multiplicity of indifferent cofounders
  8. Symptomatological basic configuration with structure tending to the chronic

Therefore an exceptionally high and diversified pathogenic potentiality exists in this mycete of just a few microns in size, which, even though it cannot be traced with the present experimental instruments, cannot be neglected from the clinical point of view.
Certainly, its present nosological classification cannot be satisfactory, because if we do not keep the possibly endless parasitic configurations in mind, that classification is too simplistic and constraining.

 

read more PART 7: FUNGAL HYPOTHESIS

Notes
9) Ibid., page 28
10) Ibid., page 29
11) Ibid., page 266
12) Ibid., page 273

 


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