Risk to children
Children that live in a household with a parent that suffers from morbid jealousy may suffer emotional and/or physical abuse as a direct result of the actions made by the parent. Children may also accidentally overhear arguments or witness physical violence between their parents. They could even be potentially accidentally injured during assaults. The morbidly jealous parent may employ a child or more than one to spy on the other parent. It is not out of the question for a child to witness a homicide or suicide where their parent is the victim. See also
References
Sources
Enoch, D. & Ball, H. (2001) The Othello Syndrome. In Enoch, D. & Ball, H. Uncommon psychiatric syndromes (fourth edition) pp50–73. London: Arnold. ISBN 0-340-76388-4

Further reading
Easton, J.A. ; Shackelford, T.K. ; Schipper, L.D. (2008). "Delusional Disorder--Jealous Type: How Inclusive are the DSM-IV Diagnostic Criteria?" (PDF). Journal of Clinical Psychology. 64 (3): 264–275. doi:10.1002/jclp.20442. PMID 18257054. Easton, J. A.; Schipper, L. D.; Shackelford, T. K. (2007). "Morbid jealousy from an evolutionary psychological perspective" (PDF). Evolution and Human Behavior. 28 (6): 399–402. doi:10.1016/j.evolhumbehav.2007.05.005. Archived from the original (PDF) on 2008-12-02.
The revised hypothesis was later formulated, in part, to accommodate reverse transcription (which both Howard Temin and David Baltimore discovered in 1970).In 1982, Stanley B. Prusiner of the University of California, San Francisco, announced that his team had purified the hypothetical infectious protein, which did not appear to be present in healthy hosts, though they did not manage to isolate the protein until two years after Prusiners announcement. The protein was named a prion, for "proteinacious infectious particle", derived from the words protein and infection. When the prion was discovered, Griffiths first hypothesis, that the protein was the product of a normally silent gene was favored by many. It was subsequently discovered, however, that the same protein exists in normal hosts but in different form.Following the discovery of the same protein in different form in uninfected individuals, the specific protein that the prion was composed of was named the prion protein (PrP), and Griffiths second hypothesis that an abnormal form of a host protein can convert other proteins of the same type into its abnormal form, became the dominant theory. Prusiner won the Nobel Prize in Physiology or Medicine in 1997 for his research into prions. See also
Diseases of abnormal polymerization
Prion pseudoknot
Subviral agents
Tau protein

References
External links

CDC – US Center for Disease Control and Prevention – information on prion diseases
World Health Organisation – WHO information on prion diseases
The UK BSE Inquiry – Report of the UK public inquiry into BSE and variant CJD
UK Spongiform Encephalopathy Advisory Committee (SEAC)