Devil facial tumor disease ( DFTD ) is an aggressively transmitted non-viral cancer that attacks Tasmanian devils, puffy animals into Australia. The DFTD was first described in 1996. In the next decade, the disease attacked the wild demons of Tasmania. The affected high-density population suffers up to 100% mortality within 12-18 months. Between 1996 and 2015, the population was reduced by 95%.
Video Devil facial tumour disease
Clinical signs
There are often more than one primary tumor. The visible signs of DFTD begin with a lump of soft tissue around the mouth, which slits. The tumor is aggressive locally, destroying the bone beneath the jaw that interferes with feeding. Tumors can also cover the eyes. Devils usually die within six months of organ failure, secondary infection, or metabolic famine. All the affected devils eventually died.
DFTD is rare in juveniles. DFTD affects men and women alike.
Maps Devil facial tumour disease
Transmission
The most plausible route of transmission is through bites, especially when the canine teeth are in direct contact with diseased cells. Other modes of transmission may include swallowing infected carcasses and food sharing, both of which involve the transfer of allogenic cells among unrelated individuals. The animals most likely to be infected are the strongest devil individuals.
Pathology
DFTD tumor is a large soft-tissue mass that becomes a central ulceration. The tumor consists of round nodule obules for spindle-shaped cells, often in pseudocapsule. The tumor metastases to the regionally involved lymph nodes and systemically to the lungs, spleen, and heart.
Characteristics of tumor
Tasmanian devil cells have 14 chromosomes; the oldest known tumor cell strain known to have thirteen chromosomes, nine of which are recognizable and four of which are "mutated" chromosomes. Newer strains evolved to have additional markers of mutant chromosomes, for a total of fourteen chromosomes. The researchers identified the cancer as a neuroendocrine tumor, and found an identical chromosome rearrangement in all cancer cells. The karyotype of DFTD cell karyotype is similar to cancer cells from canine transmissible venereal tumor (CTVT), dog cancers transmitted by physical contact. Among the mutations present in the tumor genome are trisomy on the 5p chromosome, as well as some single base mutations, and short insertions and deletions, for example, deletions on chromosomes 1, 2 and 3. Some genes mutated or deleted in DFTD are Gen RET, FANCD2 , MAST3 and BTNL9.
By 2015, the second genetically identifiable DFTD strain, the tetraploid, is not diploid like a major form of cancer. The tetraploid form has been associated with a lower mortality rate. The origin of the DFTD strain cell is unknown. Increased levels of tetraploidy have been shown to exist in the oldest DFTD strain in 2014, which correlates with the point at which the devil is involved in the DFTD removal program. Because ploidy slows the rate of tumor growth, the DFTD removal program has been suggested as a selective pressure that supports slower-growing tumors, and it is more common that disease-fighting programs aimed at DFTD can promote the evolution of DFTD. The presence of multiple strains can complicate efforts to develop vaccines, and there are reports of concerns that cancer evolution allows it to spread to related species such as quolls.
DFTD probably comes from Schwann cells from a single devil. Schwann cells are found in the peripheral nervous system, and produce myelin and other proteins that are important for the function of nerve cells in the peripheral nervous system. The researchers sampled 25 tumors and found that the tumors were genetically identical. Using deep sorting technology, the study authors then mapped out tumor transcripts, gene sequences active in tumors; transcripts are well suited to Schwann cells, revealing high activity in many genes that encode the production of myelin base proteins. Several specific markers are identified, including MBP and PRX genes, allowing veterinarians to more easily distinguish DFTD from other cancers, and ultimately can help identify a targeted genetic pathway to treat it.
Conservation response
Wild Tasmanian devil populations are being monitored to track the spread of the disease and to identify changes in the prevalence of disease. Field monitoring involves a devil's trap in a designated area to check for the presence of the disease and determine the number of affected animals. The same area is visited repeatedly to mark the spread of the disease over time. So far, it has been established that the short-term effects of disease in an area can be severe. Long-term monitoring at replicated sites will be critical to assess whether these effects persist, or whether the population can recover. Field workers also test the effectiveness of disease suppression by trapping and getting rid of the sick devils, in the hope that the removal of sick devils from wild populations will decrease the prevalence of disease, allowing the devil to survive beyond adolescence and proliferate. One study reported that the culling system before 2010 did not preclude the spread of the disease.
Selecting genetically diverse livestock seeds, determined by the genome sequence, can help conservation efforts. Two populations of "insurance" from disease-free demons have been established in urban facilities on the outskirts of Taroona and on Mary Island off the east coast of Tasmania. Captive captivity in the land zoo is also a possibility.
Because life expectancy decreases from devils with DFTD, affected individuals have begun to breed at a young age in the wild, with reports that many live only to participate in a breeding cycle. Therefore, Tasmanian devils appear to have altered breeding habits in response to the disease; The females previously started breeding every year at the age of two, for about three more years, died after various causes. The population is now characterized by the onset of breeding at one year of age, dying from DFTD, on average, shortly thereafter. Social interaction has been seen to contribute to DFTD deployment in the local area.
The decline in the number of demons is also an ecological problem, as its presence in the Tasmanian forest ecosystem is believed to have prevented the formation of the red fox, with the newest known organism unintentionally introduced to Tasmania in 1998. The young Tasmanian devil may now be more vulnerable to the predation of the red fox, the puppies are left alone for long periods of time.
In response to the impact of DFTD on the Tasmanian devil population, 47 devils have been sent to Australia's mainland wildlife park to try to preserve the genetic diversity of the species. The biggest of these efforts is the Devil Ark project at Barrington Tops, New South Wales; an initiative from Australian Reptile Park. The project aims to create a set of 1,000 genetically representative demons, and is now the main focus of the insurance policy. The Tasman Peninsula is being considered as a "clean area" that allows with a single narrow access point controlled by physical barriers. The Primary and Water Industry Department of Tasmania is experimenting to destroy the infected animals with some sign of success.
Diagnostic blood tests were developed in mid 2009 to screen for diseases. In early 2010, scientists discovered several Tasmanian devils, mostly in northwest Tasmania, which are genetically different enough for their bodies to recognize cancer as a foreign object. They have only one Main Histocompatibility Complex, while cancer cells have both.
Oocyte banking is useful in conservation efforts for Tasmanian devils, because the survival rates of cryopreserved oocytes in 70%.
History
In 1996, a photographer from the Netherlands caught several images of demons with a face tumor near Mount William in northeast Tasmania. Around the same time, farmers reported a decrease in the number of demons. Menna Jones first discovered the disease in 1999 near Little Swanport, in 2001 captured three demons with facial tumors on the Freycinet Peninsula.
The theory that cancer cells themselves can be an infective agent (Allograft Theory) was first offered in 2006 by Pearse, Swift, and colleagues, who analyzed DFTD cells from demons in several locations, which determined that all DFTD cells sampled genetically identical to each other. others, and genetically different from their hosts and from all other Tasmanian devils whose genetics have been studied; this allows them to conclude that the cancer originated from one individual and spread from it, rather than appearing repeatedly, and independently. Twenty-one different subtypes have been identified by analyzing the mitochondrial and nuclear genomes of 104 tumors from different Tasmanian devils. Researchers have also seen the previously uninfected devil develop tumors from lesions caused by infected satan bites, supporting the notion that the disease is spread by allograft, with transmission through biting, scratching, and aggressive sexual activity among individuals. During the bite, the infection can spread from a bitten demon to a bite.
Initially, it is suspected that demons have low genetic diversity, so their immune systems do not recognize tumor cells as foreign bodies. However, it was later shown that demons are quite genetically diverse to enhance a strong immune response to foreign tissue.
Since June 2005, three women have been found that are partially resistant to DFTD.
Satan's population on the peninsula dropped dramatically. In March 2003 Nick Mooney wrote memos to be circulated in Parks and Wildlife Services asking for more funds to study the disease, but a call for funding was circulated before the memo was presented to Bryan Green, then Minister of Primary Industry of Tasmania, Water and Environment. In April 2003, a working group was formed by the Tasmanian Government to respond to the disease. In September 2003, Nick Mooney went to the Tasmanian daily newspaper The Mercury, informing the public about the disease and proposing a healthy Tasmanian devil quarantine. At that time, it was considered that retroviruses were the possible cause. David Chadwick of the State Animal Health laboratory said that the lab did not have the resources needed to investigate retrovirus possibilities. The Tasmanian Conservation Trust criticized the Tasmanian government for providing insufficient funds for research and suggested that DFTD could become a zoonotic, which poses a threat to livestock and humans. On October 14, 2003, a workshop was held in Launceston. In 2004, Kathryn Medlock discovered three odd-shaped demons in European museums and found a vicious description of the devil at the London Zoo, which showed a resemblance to the DFTD.
Calicivirus, 1080 poison, agricultural chemicals, and habitat fragmentation combined with retroviruses are another proposed cause. Environmental toxins have also been suspected. In March 2006 the devil escaped from a park to an area infected with DFTD. He was recaptured with a bite mark on his face, and returned to live with another demon in the park. He injured a man and in October the two devils possessed the DFTD, which then spread to the other two (an incident that in retrospect would be understood in the context of the allograft transmission theory).
In 2006, DFTD was classified as a disease listed in List B under the Tasmanian Government Animal Health Act 1995. The development strategy of the insurance population in captivity was developed. It was reassessed in 2008. A 2007 investigation of Satan's immune system found that when fighting other pathogens, the response of the immune system is normal, leading to the suspicion that Satan is unable to detect cancer cells as "non-self". In 2007, it was predicted that the population could become extinct locally within 10-15 years after the DFTD occurred, and predicted that the disease would spread throughout the Tasmanian devils range causing the devil to become extinct within 25-35 years.
By 2016, the devil is on the brink of extinction as the local population has declined by 90 percent and the overall decline of the species by more than 80 percent in less than 20 years, with some models predicting extinction. Nonetheless, the devil population survives in the affected area. Satan, by the way, is resisting extinction by developing genes that are immune to tumors. Genes already exist in Tasmanian devils as part of their immune system. They are increasing in frequency due to natural selection. That is, individuals with certain forms of this gene (allele) survive and are reproduced disproportionately to those who do not have a specific variant when the disease is present.
Satanic populations in the southwestern tip of Tasmania have been reported to be free of DFTD.
Society and culture
In 2008, the devil - named Cedric by those who treated and worked with him - was considered to have natural immunity against the disease, but developed two facial tumors by the end of 2008. The tumor was removed, and officials thought Cedric recovered well; but in September 2010, the cancer was found to spread to the lungs, which caused her euthanasia.
Direction of research
Vaccination with irradiated cancer cells has not been proven successful.
In 2013, a study using rats as a model for Tasmanian devils suggested that DFTD vaccine could be useful. By 2015, a study that mixes DFTD cells that die with an inflammatory substance stimulates an immune response in five of the six demons injected with the mixture, which produces a vaccine against DFTD. Field trials of a potential vaccine are underway as a collaborative project between the Menzies Institute for Medical Research and the Save the Tasmanian Devil Program under the Wild Devil Recovery program, and aims to test immunization protocols as a tool to ensure long-term satanic survival in the wild.
In March 2017, scientists at the University of Tasmania presented the first clear report after successfully treating Tasmanian devils with this disease, by injecting live cancerous cells into infected demons to stimulate their immune systems to recognize and fight disease.
References
External links
- Devil Ark conservation project
Source of the article : Wikipedia
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