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User:ChoLi8/Conservation Biology

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Illustration ideas

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A. A map of the range of the cancer affecting the California Sea Lions

B. A schematic of the biochemistry of the cancer

C. An illustration of a sea lion with the cancer

Genital Carcinoma of California Sea lions

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Outline

I. Introduction/Overview

II. Biochemistry

A. Viral causes
B. Other causes

III. Human Influences

A. Pollution
B. Toxic chemicals

IV. Ecological Effects

A. Physical effects on the sea lions
B. Range and statistics of the cancer

V. Conservation Efforts

Discovery

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In 1996, a research group lead by Dr. Frances Gulland, examined 370 sub-adult and adult California sea lions between January 1979 and December 1999.[1] The number of cancer related cases was high, it was found that around 18 percent of all stranded adult sea lion deaths were cancer related.[1]

Characteristics

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Sea lions with the carcinoma, in the 1996 study, were clinically characterized by emaciation, anorexia, and to some degree, paralysis of the hind flippers. In addition, there would often be swelling of the hind flippers and perineal edema.[1] Large cancerous masses up to 25 cm in diameter and 2.8 kg in weight were present in the pelvic area. These masses were mainly involved in the sublumbar lymph nodes, around ureters, and, sometimes, the adrenal glands, kidneys, and bladder. Masses in the kidney, bladder, and reproductive tract were the least frequent. Metastasized tumor cells were also found within the lungs, colon, spleen and liver. Many of the tumor metastases, especially those within lymph nodes, had necrotic centers with granular, eosinophillic cell debris and deteriorated neutrophils.

Neoplastic cells, mostly, were arranged in small nests and sheets and were usually found in small vessels and lymphatic channels.[1]Cell cytoplasm was pale; eosinophillic and amphophillic while cell nuclei varied from 8 to 15 micrometers in diameter. The nuclei had a clumped and reticular chromatin pattern. Mitosis of the cells was generally infrequent. Upon immunohistochemical studies, it was determined that the neoplastic cells to be epithelial in origin.

Chemical and Anthropogenic Reasons

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There has been evidence that organochlorines may play a part in the high prevalence of cancer cases, including those involving the urogenital tracts.[2] Probability of death by cancer was determined to increase when organochlorine tissue concentrations increased. Sea lions that died from cancer related causes had higher mean concentrations of the organochlorines, PCB and DDT, by more than 80 and 30 percent, respectively, in the blubber. PCB and DDT concentrations are monitored from blubber because of their lipophilic natures.[3] Male sea lions affected by cancer had the highest concentration of organochlorines. When blubber thickness data was controlled for the study, only PCB concentration was seen to significantly affect probability of cancer death while DDT concentration was not significant.[2]

Adult female California sea lions were found to have lower concentration of the organochlorines than adult male sea lions, pups, and yearlings with the greatest difference in organochlorine concentration between the pups and adult female sea lions.[4] The rationale behind the high organochlorine concentration in pups is that the Southern California bight is a key breeding site where organochlorine, lipophilic in nature, may be absorbed through maternal lipid stores during gestation and lactation. In addition, pups are nursed in the bight for up to 11 months.

Research has also found that DDT concentration is higher than PCB concentration in California sea lions compared to elephant and harbor seal PCB and DDT concentrations in the California coast.[3] DDT concentration is higher than PCB concentration in elephant and harbor seals.

South California manufacturers have contributed to elevated PCB and DDT concentrations in the waters of Southern California through discharge, such as the sewer systems.[5] In the 1970s, the manufacturing and use of PCB and DDT was banned in the United States by the Environmental Protection Agency (EPA). Since that action, emissions of these highly toxic chemicals have rapidly dropped in the United States. From 1931 to 1973, fourteen dump sites were designated for waste disposal for a variety of materials into the Southern California seas. The EPA has made some of the sites illegal for dumping and others for use for the Army Corps of Engineers. The increase of pollutants in the 1940s to 1970s has scientists speculating that this case of carcinogenesis of the sea lion may be anthropogenically related.[6] Interestingly, PCBs have been investigated to have carcinogenic characteristics [7] while DDT’s effect in increasing cancer risk is still being debated.[8] The current concentrations of PCB and DDT are among the highest values reported in the world for marine mammals and exceed reported concentrations that cause harmful health effects.[4]

Viral Reasons

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A study in 2000, suggested that a novel gammaherpesvirus is a possible cause of California sea lion carcinoma of genital origin.[9] Tissue samples werecollected from ten adult California sea lions, seven females and three males, that had metastasized carcinoma in sublumbar area lymph nodes and were histologically examined. Viral particles consistent with those of a herpesvirus were found through electron microscope examination of tissue sample from two sea lions with intra-epithelial neoplasia and metastatic carcinoma respectfully. In addition, an immunohistochemical stain was positive for the latent membrane of Epstein-Barr virus, a herpes virus with cancer causing ties, in another intra-epithelial neoplasia tissue sample. DNA samples from four metastatic carcinomas were positive for herpesvirus DNA sequences by polymerase chain reaction (PCR).

After the discovery of the novel gammaherpesvirus, phylogenetic analysis grouped the virus, designated Otarine herpesvirus-1 (OtHV-1) within the gammaherpesvirus subfamily.[10] A PCR specific for OtHV-1 was used to investigate its presence in 16 individual California sea lion tumor tissue samples and was found present in 100 percent of tumors. In addition, DNA extracted from archived sea lion brain and muscle tissues was also positive for OtHV-1 in 29 and 50 percent, respectively, of a sample group of 14. In 2006, a study reported that the herpesvirus was 100 percent prevalent and more widespread in 15 California sea lions with urogenital carcinoma than samples taken from 25 controls.[11] The virus was mostly found in the urogenital tissues and draining lymph nodes. Interestingly, OtHV-1 DNA was not found in any juvenile sea lions or neoplastic tissues of sea lions with non-urogenital tumors. The prevalence of the virus in adults but lack of in juveniles may suggest that the OtHV-1 infection is acquired through breeding [11][12]. Sexual reproduction has been a platform for the spreading of other known herpesviruses.

Genetic Reasons

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Inbreeding is known to increase susceptibility to pathogens, such as herpesviruses, and in the case of urogenital carcinoma, researchers have found that California sea lions afflicted with the cancer have higher than normal parental relatedness.[13] The more inbred sea lions were found to respond to treatment for recovery slower than less inbred sea lions.

Immunogenetic basis

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The important major histocompatibility complex (MHC) gene has associations with cancer that are well established in the cancer biology literature.[14] MHC genotypes have been examined from 27 cancer positive and 22 cancer negative stranded California sea lions using a sequence specific primer-based PCR with intercalating dye technology. The analysis elucidated an immunogenetic component for the high prevalence of urogenital carcinoma in California sea lions. Upon comparing between the genotypes of stranded animals with and without cancer, the presence of the MHC class II locus, Zaca-DRB.A, was strongly associated with an increased risk of cancer in the stranded sea lions. Thus, the presence of class II MHC genes may increase cancer risk in the sea lions. More research with larger sample sizes is needed as well as more research for the elucidation of a potential mechanism and further understanding of the interactions of immunogenetic factors, chemical pollutants, and pathogenic factors.

References

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  1. ^ a b c d Gulland, F.M., J.G. Trupkiewicz, T.R. Spraker, and L.J. Lowenstine, Metastatic carcinoma of probable transitional cell origin in 66 free-living California sea lions (Zalophus californianus). 1979 to 1994. J Wildl Dis, 1996. 32(2): p. 250-8.
  2. ^ a b Ylitalo, G.M., J.E. Stein, T. Hom, L.L. Johnson, K.L. Tilbury, A.J. Hall, T. Rowles, D. Greig, L.J. Lowenstine, and F.M. Gulland, The role of organochlorines in cancer-associated mortality in California sea lions (Zalophus californianus). Mar Pollut Bull, 2005. 50(1): p. 30-9.
  3. ^ a b Kajiwara N., et al., Organochlorine Pesticides, Polychlorinated Biphenyls, and Butyltin Compounds in Blubber and Livers of Stranded California Sea Lions, Elephant Seals, and Harbor Seals from Coastal California, USA. Archives of Environmental Contamination and Toxicology Volume 41, Number 1, 90-99.
  4. ^ a b Blasius M. E., Goodmanlowe G.D., Contaminants still high in top-level carnivores in the Southern California Bight: Levels of DDT and PCB in resident and transient pinnipeds, Marine Pollution Bulletin, Volume 56, Issue 12, December 2008, Pages 1973-1982.
  5. ^ “Panel on Southern California Bight of the Committee on a Systems Assessment of Marine Environmental Monitoring”, . Monitoring Southern California's Coastal Waters. Washing ton D.C.: National Academy Press, 1990. 31-35. eBook. <http://www.nap.edu/openbook.php?record_id=1607&page=35>.
  6. ^ Chen, Ingfei. "Cancer Kills Many Sea Lions, and Its Cause Remains a Mystery." New York Times 4 March 2010, n. pag. Web. 1 Dec. 2011. <http://www.nytimes.com/2010/03/05/science/05sfsealion.html?pagewanted=all>.
  7. ^ Faroon, O.M., S. Keith, D. Jones, and C. De Rosa, Carcinogenic effects of polychlorinated biphenyls. Toxicol Ind Health, 2001. 17(2): p. 41-62.
  8. ^ Rogan WJ, Chen A., Health risks and benefits of bis(4-chlorophenyl)-1,1,1-trichloroethane (DDT). Lancet, 2005. 366 (9487): 763–73.
  9. ^ Lipscomb, T.P., D.P. Scott, R.L. Garber, A.E. Krafft, M.M. Tsai, J.H. Lichy, J.K. Taubenberger, F.Y. Schulman, and F.M. Gulland, Common metastatic carcinoma of California sea lions (Zalophus californianus): evidence of genital origin and association with novel gammaherpesvirus. Vet Pathol, 2000. 37(6): p. 609-17.
  10. ^ King, D.P., M.C. Hure, T. Goldstein, B.M. Aldridge, F.M. Gulland, J.T. Saliki, E.L. Buckles, L.J. Lowenstine, and J.L. Stott, Otarine herpesvirus-1: a novel gammaherpesvirus associated with urogenital carcinoma in California sea lions (Zalophus californianus). Vet Microbiol, 2002. 86(1-2): p. 131-7.
  11. ^ a b Buckles, E.L., L.J. Lowenstine, C. Funke, R.K. Vittore, H.N. Wong, J.A. St Leger, D.J. Greig, R.S. Duerr, F.M. Gulland, and J.L. Stott, Otarine Herpesvirus-1, not papillomavirus, is associated with endemic tumours in California sea lions (Zalophus californianus). J Comp Pathol, 2006. 135(4): p. 183-9.
  12. ^ Buckles, E.L., L.J. Lowenstine, R.L. DeLong, S.R. Melin, R.K. Vittore, H.N. Wong, G.L. Ross, J.A. St Leger, D.J. Greig, R.S. Duerr, F.M. Gulland, and J.L. Stott, Age-prevalence of Otarine Herpesvirus-1, a tumor-associated virus, and possibility of its sexual transmission in California sea lions. Vet Microbiol, 2007. 120(1-2): p. 1-8.
  13. ^ Acevedo-Whitehouse, K., F. Gulland, D. Greig, and W. Amos, Inbreeding: Disease susceptibility in California sea lions. Nature, 2003. 422(6927): p. 35.
  14. ^ Bowen, L., B.M. Aldridge, R. Delong, S. Melin, E.L. Buckles, F. Gulland, L.J. Lowenstine, J.L. Stott, and M.L. Johnson, An immunogenetic basis for the high prevalence of urogenital cancer in a free-ranging population of California sea. Immunogenetics (2005) 56: 846–848.
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