Introduction
Devil facial tumour disease (DFTD) is a transmissible non-viral parasitic cancer (Pyecroft et al. 2007). It is believed to originate from Tasmanian devils’ Schwann cells. The disease was first reported in Australia in 1996. It vastly attacked Tasmania’s wild devils in the subsequent decade and increased their death rate from 20% to about 50%. Its symptoms begin with lumps and lesions around the mouth, and then turn into cancerous tumors that can be infected to the rest of the body. Since 1996, the incidence the disease has grown to over 70%, with the devils’ behavior of biting each other when feeding intensifying its transmission (McCallum & Jones 2006; Jones et al 2008). The purpose of this article is to have a better understanding on the pathology, epidemiology, and fundamental immunological DFTD foundation.
Discussion
The disease is a type of cancer that is extremely aggressive and which attacks the facial tissues. Presently, it is feared that if it continues at its worrying rate, it might lead to critical extinction of the Tasmanian devils’ population. Its histogenesis has not yet been certainly established, but it is probable that it originated from a cell-lineage of neural crest (Loh et al. 2006). It is also believed that the disease is being spread through biting as the animals interact socially – this transmission happens as a tumor ‘allagraft’ between individual animals (Loh et al. 2006).
The transmission of DFTD across the species is thought to be enhanced by a declined MHC diversity, most likely resulting from a bottleneck evolution. “The pathogenesis of DFTD has some similarities with certain human cancers, including donor-recipient tumor transmission, which may complicate organ transplantation and certain forms of malignancy at the maternal/fetal interface, makes organ transplantation very difficult” (Loh et al. 2006, p. 12).
It has been confirmed that the animals are quite common and have inhabited a big space across Tasmania, Australia (Hawkins, 2006). The population of this species has declined significantly, which is attributable to DFTD devastation (Lachish, McCallum & Jones 2009; McCallum & Jones 2006; Jones et al 2008). Giving in on tumor surveillance as a result of MHC diversity may be a basis for immunology for this condition (Siddle et al 2007); however, substantiation on this procedure requires further research. Certainly, pathogenesis of DFTD is a critical issue for conserving the species. It is an important issue because of its similarity with some cancers of the human beings, therefore, providing an innovative and a complementary approach for surveillance of tumor immune, which can be used constructively by oncologists who deal with immunology of tumor (Stephen et al. 2006)
Conclusion
The pathology, epidemiology and probable foundation for DFTD immunology gives insights into a very strange malignant development. Transmission of DFTD across the species is thought to be responsible for the declined MHC diversity, probably due to a bottleneck evolution. The understanding of the fundamental biology behind this disease is mounting; however, the survival of the remaining Tasmanian devil population as a result of this devastation is highly unclear, though it is probable that the disease poses a very serious extinction risk for the animals (Jones et al 2008; Obendorf & McGlashan 2008; McCallum & Jones 2006; Jones et al 2008). Nevertheless, there are some developments aimed at reducing the transmission of the disease and safeguarding the species (Obendorf & McGlashan 2008; Save the Tasmanian devil n.d.).
References
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