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{{Rubella}}
{{Rubella}}
{{CMG}}
{{CMG}}
 
{{MJM}}
==Overview==
==Overview==


==Natural history==
==Natural history==
Rubella was first described in the mid-eighteenth century. [[Friedrich Hoffmann]] made the first clinical description of rubella in 1740,<ref name=Ackerknecht1982>{{cite book |author=Ackerknecht, Erwin Heinz |title=A short history of medicine |publisher=Johns Hopkins University Press |location=Baltimore |year=1982 |pages=129 |isbn=0-8018-2726-4}}</ref> which was confirmed by de Bergen in 1752 and Orlow in 1758.<ref name="pmid18109609">{{cite journal
|author=Wesselhoeft C
|title=Rubella and congenital deformities
|journal=N. Engl. J. Med.
|volume=240
|issue=7
|pages=258–61
|year=1949
|pmid=18109609
|doi=
}}</ref>
In 1814, George de Maton first suggested that it be considered a disease distinct from both measles and scarlet fever. All these physicians were German, and the disease was known  as Rötheln (from the German name ''Röteln''), hence the common name of "German measles". <ref>Best, J.M., Cooray, S.,  Banatvala J.E. '''Rubella''' in ''Topley and Wilson's Microbiology and Microbial Infections'', Vol. 2, Virology, Chapter 45, p.960-92, ISBN 0 340 88562 9, 2005 </ref> Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name "rubella" (from the Latin, meaning "little red") in 1866.<ref name=Ackerknecht1982/><ref name=Lee2000>{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=Clin. Microbiol. Rev. |volume=13 |issue=4 |pages=571-87 |year=2000 |pmid=11023958 |url=http://cmr.asm.org/cgi/content/full/13/4/571}}</ref><ref name=cdc>{{cite book
| author = Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds.
| year = 2007
| url = http://www.cdc.gov/vaccines/pubs/pinkbook/pink-chapters.htm
| title = Epidemiology and Prevention of Vaccine-Preventable Diseases. 10th ed.
| chapter = Chapter 12. Rubella
| chapterURL = http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/rubella.pdf
| publisher = Centers for Disease Control and Prevention
| accessdate = 2007-07-03
}}</ref><ref name=MoHNZ>{{cite book
| year = 2006
| month = April
| title = Immunisation Handbook 2006
| publisher = Ministry of Health, Wellington, NZ.
| url = http://www.moh.govt.nz/moh.nsf/indexmh/immunisation-handbook-2006
| chapter = Chapter 11 - Rubella
| chapterURL = http://www.moh.govt.nz/moh.nsf/pagesmh/4617/$File/2006-11rubella.pdf
| isbn=0-478-29926-5
| accessdate = 2007-07-03
}}</ref>
It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.<ref>Smith, J. L. Contributions to the study of Rötheln. Trans. Int. Med. Congr. Phil. '''4''',14. 1881</ref> In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.<ref name=whonamedit>{{cite journal
| first = Alfred Fabian
| last = Hess
| year = 1914
| title = German measles (rubella): an experimental study
| journal = The Archives of Internal Medicine
| location = Chicago
| volume = 13
| pages = 913-916
}} as cited by {{cite web
| first = Ole Daniel
| last = Enersen
| url = http://www.whonamedit.com/doctor.cfm/2283.html
| title = Alfred Fabian Hess
| publisher = WhoNamedIt
| accessdate = 2007-07-03
}}</ref> In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.<ref name=cdc/>
In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella in early pregnancy.<ref name=Lee2000/><ref name=cdc/> Gregg published an account, ''Congenital Cataract Following German Measles in the Mother'', in 1941. He described a variety of problems now know as [[congenital rubella syndrome]] (CRS) and noticed that the earlier the mother was infected, the worse the damage was. The virus was isolated in tissue culture in 1962 by two separate groups led by physicians Parkman and Weller.<ref name=MoHNZ/><ref name=Lee2000/>
There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.<ref name=MoHNZ/> In the years 1964-65, the United States had an estimated 12.5 million rubella cases. This led to 11,000 miscarriages or therapeutic abortions and 20,000 cases of congenital rubella syndrome. Of these, 2,100 died as neonates, 12,000 were deaf, 3,580 were blind and 1,800 were mentally retarded. In New York alone, CRS affected 1% of all births <ref> J.B. Hanshaw, J.A. Dudgeon, and W.C. Marshall. Viral diseases of the fetus and newborn. W.B. Saunders Co., Philadelphia, 1985 </ref>
In 1969 a live attenuated virus vaccine was licensed.<ref name=cdc/> In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.<ref name=MoHNZ/>


==Complications==
==Complications==
Rubella can cause a wide variety of problems that are seen very commonly with rubella or not very often at all. Two of the more common complications that occur with the rubella virus are [[arthralgia]] and [[arthritis]]. For currently unknown reasons, the symptoms that were just mentioned are found to be more prevalent in women with the rubella virus than with men with the rubella virus<ref name="pmid11023958">{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=[[Clinical Microbiology Reviews]] |volume=13 |issue=4 |pages=571–87 |year=2000 |month=October |pmid=11023958 |pmc=88950 |doi= |url=http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=11023958 |accessdate=2012-02-09}}</ref>. There are also some more serious complications associate with the rubella virus. One of these complications is [[thrombocytopenic purpura]], which is a disorder with the blood. It causes extensive microscopic [[clots]] to form in the small blood vessels of the body. Before effective treatment was developed, the fatality rate was approximately 90%.
Another complication associated with the rubella virus is [[postinfectious encephalopathy]] or [[encephalomyelitis]]. Encephalomyelitis is basically just a general term for [[inflammation]] of the [[brain]] and [[spinal cord]]. It should be noted, though, that encephalomyelitis and thrombocytopenic purpura are rarely associated with postnatally developed rubella<ref name="pmid11023958">{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=[[Clinical Microbiology Reviews]] |volume=13 |issue=4 |pages=571–87 |year=2000 |month=October |pmid=11023958 |pmc=88950 |doi= |url=http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=11023958 |accessdate=2012-02-09}}</ref>.
Probably the most major concern, and public health concern, associated with rubella is its [[teratogenicity]]. The length of [[gestation]] when a mother contracts rubella plays a major factor in determining which [[congenital]] defects may be possible.  If the woman contracts rubella earlier in her [[pregnancy]], then there is a higher chance of her child developing serious defects<ref name="pmid11023958">{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=[[Clinical Microbiology Reviews]] |volume=13 |issue=4 |pages=571–87 |year=2000 |month=October |pmid=11023958 |pmc=88950 |doi= |url=http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=11023958 |accessdate=2012-02-09}}</ref>. Nearly 100% of fetuses become infected when a mother contracts the disease within the first 8 weeks of pregnancy<ref name="pmid11023958">{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=[[Clinical Microbiology Reviews]] |volume=13 |issue=4 |pages=571–87 |year=2000 |month=October |pmid=11023958 |pmc=88950 |doi= |url=http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=11023958 |accessdate=2012-02-09}}</ref>. After approximately 17 weeks (the first [[trimester]]), contracting rubella will most likely not have consequences on the child.
Some of the complications that have been reported with the child include<ref name="pmid11023958">{{cite journal |author=Lee JY, Bowden DS |title=Rubella virus replication and links to teratogenicity |journal=[[Clinical Microbiology Reviews]] |volume=13 |issue=4 |pages=571–87 |year=2000 |month=October |pmid=11023958 |pmc=88950 |doi= |url=http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=11023958 |accessdate=2012-02-09}}</ref>. :
*[[Deafness]]
*[[Cardiac disease]]
*[[Mental retardation]]
*[[Ocular]] conditions including
**[[Cataracts]]
**[[Glaucoma]]
*[[Insulin]] dependent [[diabetes mellitus]]
It should be noted that there have been no cases ''reported'' of rubella infection causing [[congenital rubella syndrome]] after 12 weeks gestation.


==Prognosis==
==Prognosis==
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==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
  complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Michael Maddaleni, B.S.

Overview

Natural history

Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740,[1] which was confirmed by de Bergen in 1752 and Orlow in 1758.[2]

In 1814, George de Maton first suggested that it be considered a disease distinct from both measles and scarlet fever. All these physicians were German, and the disease was known as Rötheln (from the German name Röteln), hence the common name of "German measles". [3] Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name "rubella" (from the Latin, meaning "little red") in 1866.[1][4][5][6]

It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.[7] In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.[8] In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.[5]

In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella in early pregnancy.[4][5] Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now know as congenital rubella syndrome (CRS) and noticed that the earlier the mother was infected, the worse the damage was. The virus was isolated in tissue culture in 1962 by two separate groups led by physicians Parkman and Weller.[6][4]

There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.[6] In the years 1964-65, the United States had an estimated 12.5 million rubella cases. This led to 11,000 miscarriages or therapeutic abortions and 20,000 cases of congenital rubella syndrome. Of these, 2,100 died as neonates, 12,000 were deaf, 3,580 were blind and 1,800 were mentally retarded. In New York alone, CRS affected 1% of all births [9]

In 1969 a live attenuated virus vaccine was licensed.[5] In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.[6]

Complications

Rubella can cause a wide variety of problems that are seen very commonly with rubella or not very often at all. Two of the more common complications that occur with the rubella virus are arthralgia and arthritis. For currently unknown reasons, the symptoms that were just mentioned are found to be more prevalent in women with the rubella virus than with men with the rubella virus[10]. There are also some more serious complications associate with the rubella virus. One of these complications is thrombocytopenic purpura, which is a disorder with the blood. It causes extensive microscopic clots to form in the small blood vessels of the body. Before effective treatment was developed, the fatality rate was approximately 90%.

Another complication associated with the rubella virus is postinfectious encephalopathy or encephalomyelitis. Encephalomyelitis is basically just a general term for inflammation of the brain and spinal cord. It should be noted, though, that encephalomyelitis and thrombocytopenic purpura are rarely associated with postnatally developed rubella[10].

Probably the most major concern, and public health concern, associated with rubella is its teratogenicity. The length of gestation when a mother contracts rubella plays a major factor in determining which congenital defects may be possible. If the woman contracts rubella earlier in her pregnancy, then there is a higher chance of her child developing serious defects[10]. Nearly 100% of fetuses become infected when a mother contracts the disease within the first 8 weeks of pregnancy[10]. After approximately 17 weeks (the first trimester), contracting rubella will most likely not have consequences on the child.

Some of the complications that have been reported with the child include[10]. :

It should be noted that there have been no cases reported of rubella infection causing congenital rubella syndrome after 12 weeks gestation.

Prognosis

Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.[11]

References

  1. 1.0 1.1 Ackerknecht, Erwin Heinz (1982). A short history of medicine. Baltimore: Johns Hopkins University Press. p. 129. ISBN 0-8018-2726-4.
  2. Wesselhoeft C (1949). "Rubella and congenital deformities". N. Engl. J. Med. 240 (7): 258–61. PMID 18109609.
  3. Best, J.M., Cooray, S., Banatvala J.E. Rubella in Topley and Wilson's Microbiology and Microbial Infections, Vol. 2, Virology, Chapter 45, p.960-92, ISBN 0 340 88562 9, 2005
  4. 4.0 4.1 4.2 Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clin. Microbiol. Rev. 13 (4): 571–87. PMID 11023958.
  5. 5.0 5.1 5.2 5.3 Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. (2007). "Chapter 12. Rubella". Epidemiology and Prevention of Vaccine-Preventable Diseases. 10th ed. Centers for Disease Control and Prevention. Retrieved 2007-07-03. Unknown parameter |chapterURL= ignored (|chapterurl= suggested) (help)
  6. 6.0 6.1 6.2 6.3 "Chapter 11 - Rubella". Immunisation Handbook 2006. Ministry of Health, Wellington, NZ. 2006. ISBN 0-478-29926-5. Retrieved 2007-07-03. Unknown parameter |month= ignored (help); Unknown parameter |chapterURL= ignored (|chapterurl= suggested) (help)
  7. Smith, J. L. Contributions to the study of Rötheln. Trans. Int. Med. Congr. Phil. 4,14. 1881
  8. Hess, Alfred Fabian (1914). "German measles (rubella): an experimental study". The Archives of Internal Medicine. Chicago. 13: 913–916. as cited by Enersen, Ole Daniel. "Alfred Fabian Hess". WhoNamedIt. Retrieved 2007-07-03.
  9. J.B. Hanshaw, J.A. Dudgeon, and W.C. Marshall. Viral diseases of the fetus and newborn. W.B. Saunders Co., Philadelphia, 1985
  10. 10.0 10.1 10.2 10.3 10.4 Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clinical Microbiology Reviews. 13 (4): 571–87. PMC 88950. PMID 11023958. Retrieved 2012-02-09. Unknown parameter |month= ignored (help)
  11. Freij BJ, South MA, Sever JL (1988). "Maternal rubella and the congenital rubella syndrome". Clin Perinatol. 15 (2): 247–57. PMID 3288422.
 complications and prognosis