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Rubella
Classification and external resources
Template:Px
ICD-10 B06
ICD-9 056
DiseasesDB 11719
MedlinePlus 001574
eMedicine emerg/388 peds/2025 derm/259
MeSH D012409

Rubella, commonly known as German measles, is a disease caused by the rubella virus. The name "rubella" is derived from the Latin, meaning little red. Rubella is also known as German measles because the disease was first described by German physicians in the mid-eighteenth century. This disease is often mild and attacks often pass unnoticed. The disease can last one to three days. Children recover more quickly than adults. Infection of the mother by Rubella virus during pregnancy can be serious; if the mother is infected within the first 20 weeks of pregnancy, the child may be born with congenital rubella syndrome (CRS), which entails a range of serious incurable illnesses. Spontaneous abortion occurs in up to 20% of cases.[1]

Rubella is a common childhood infection usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection.

Acquired (i.e. not congenital) rubella is transmitted via airborne droplet emission from the upper respiratory tract of active cases. The virus may also be present in the urine, feces and on the skin. There is no carrier state: the reservoir exists entirely in active human cases. The disease has an incubation period of 2 to 3 weeks.[2]

In most people the virus is rapidly eliminated. However, it may persist for some months post partum in infants surviving the CRS. These children are a significant source of infection to other infants and, more importantly, to pregnant female contacts.

It should not be confused with rubeola, which was a historical name for measles.

Signs and symptoms

After an incubation period of 14–21 days, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days. Other symptoms include low grade fever, swollen glands (post cervical lymphadenopathy), joint pains, headache and conjunctivitis.[3] The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 oC (100.4 oF). The rash disappears after a few days with no staining or peeling of the skin. Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.

Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to one-third of older girls or women experience joint pain or arthritic type symptoms with rubella. The virus is contracted through the respiratory tract and has an incubation period of 2 to 3 weeks. During this incubation period, the carrier is contagious but may show no symptoms.

Congenital rubella syndrome

Main article: Congenital rubella syndrome

Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects.[4] It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anaemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed. Many mothers who contract rubella within the first critical trimester either have a miscarriage or a still born baby. If the baby survives the infection, it can be born with severe heart disorders (PDA being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called "blueberry muffin lesions." [5]

Cause

The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome.[6] The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. It is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.[3]

Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are be involved in virus infection or non-resolution of the disease.[7] [8]

Diagnosis of acquired rubella

Rubella virus specific IgM antibodies are present in people recently infected by Rubella virus but these antibodies can persist for over a year and a positive test result needs to be interpreted with caution.[9] The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.[10]

Prevention

Main article: MMR vaccine

Rubella infections are prevented by active immunisation programs using live, disabled virus vaccines. Two live attenuated virus vaccines, RA 27/3 and Cendehill strains, were effective in the prevention of adult disease. However their use in prepubertile females did not produce a significant fall in the overall incidence rate of CRS in the UK. Reductions were only achieved by immunisation of all children.

The vaccine is now given as part of the MMR vaccine. The WHO recommends the first dose is given at 12 to 18 months of age with a second dose at 36 months. Pregnant women are usually tested for immunity to rubella early on. Women found to be susceptible are not vaccinated until after the baby is born because the vaccine contains live virus.[11]

The immunization program has been quite successful. Cuba declared the disease eliminated in the 1990s, and in 2004 the Centers for Disease Control and Prevention announced that both the congenital and acquired forms of rubella had been eliminated from the United States.[12][13]

Treatment

There is no specific treatment for Rubella; management is a matter of responding to symptoms to diminish discomfort. Treatment of newly born babies is focused on management of the complications. Congenital heart defects[How to reference and link to summary or text] and cataracts can be corrected by surgery.[14] Management for ocular CRS is similar to that for age-related macular degeneration, including counseling, regular monitoring, and the provision of low vision devices, if required.[15]

Prognosis

Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.[16]

Epidemiology

Rubella is a disease that occurs worldwide. The virus tends to peak during the spring in countries with temperate climates. Before the vaccine to rubella was introduced in 1969, widespread outbreaks usually occurred every 6–9 years in the United States and 3–5 years in Europe, mostly affecting children in the 5-9 year old age group.[17] Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates. However, in the UK there remains a large population of men susceptible to rubella who have not been vaccinated. Outbreaks of rubella occurred amongst many young men in the UK in 1993 and in 1996 the infection was transmitted to pregnant women, many of whom were immigrants and were susceptible. Outbreaks still arise, usually in developing countries where the vaccine is not as accessible.[18]

During the epidemic in the US between 1962-1965, Rubella virus infections during pregnancy were estimated to have caused 30,000 still births and 20,000 children to be born impaired or disabled as a result of CRS.[19][20] Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.[21]

History

Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740,[22] which was confirmed by de Bergen in 1752 and Orlow in 1758.[23]

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". [24] 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.[22][25][26][27]

It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.[28] In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.[29] In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.[26]

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.[25][26] Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now known 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.[25][27]

There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.[27] 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 [30]

In 1969 a live attenuated virus vaccine was licensed.[26] In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.[27]

See also


References

  1. Siegel M, Fuerst HT, Guinee VF (1971). Rubella epidemicity and embryopathy. Results of a long-term prospective study. Am. J. Dis. Child. 121 (6): 469–73.
  2. Richardson M, Elliman D, Maguire H, Simpson J, Nicoll A (2001). Evidence base of incubation periods, periods of infectiousness and exclusion policies for the control of communicable diseases in schools and preschools. Pediatr. Infect. Dis. J. 20 (4): 380–91.
  3. 3.0 3.1 Edlich RF, Winters KL, Long WB, Gubler KD (2005). Rubella and congenital rubella (German measles). J Long Term Eff Med Implants 15 (3): 319–28.
  4. Atreya CD, Mohan KV, Kulkarni S (2004). Rubella virus and birth defects: molecular insights into the viral teratogenesis at the cellular level. Birth Defects Res. Part a Clin. Mol. Teratol. 70 (7): 431–7.
  5. De Santis M, Cavaliere AF, Straface G, Caruso A (2006). Rubella infection in pregnancy. Reprod. Toxicol. 21 (4): 390–8.
  6. Frey TK (1994). Molecular biology of rubella virus. Adv. Virus Res. 44: 69–160.
  7. Forrest JM, Turnbull FM, Sholler GF, et al. (2002). Gregg's congenital rubella patients 60 years later. Med. J. Aust. 177 (11-12): 664–7.
  8. Honeyman MC, Dorman DC, Menser MA, Forrest JM, Guinan JJ, Clark P (February 1975). HL-A antigens in congenital rubella and the role of antigens 1 and 8 in the epidemiology of natural rubella. Tissue Antigens 5 (1): 12–8.
  9. Best JM (2007). Rubella. Semin Fetal Neonatal Med 12 (3): 182–92.
  10. Stegmann BJ, Carey JC (2002). TORCH Infections. Toxoplasmosis, Other (syphilis, varicella-zoster, parvovirus B19), Rubella, Cytomegalovirus (CMV), and Herpes infections. Curr Women's Health Rep 2 (4): 253–8.
  11. Watson JC, Hadler SC, Dykewicz CA, Reef S, Phillips L (1998). Measles, mumps, and rubella--vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 47 (RR-8): 1–57.
  12. Dayan GH, Castillo-Solórzano C, Nava M, et al. (2006). Efforts at rubella elimination in the United States: the impact of hemispheric rubella control. Clin. Infect. Dis. 43 Suppl 3: S158–63.
  13. (2005)Elimination of rubella and congenital rubella syndrome--United States, 1969-2004. MMWR Morb. Mortal. Wkly. Rep. 54 (11): 279–82.
  14. Khandekar R, Sudhan A, Jain BK, Shrivastav K, Sachan R (2007). Pediatric cataract and surgery outcomes in Central India: a hospital based study. Indian J Med Sci 61 (1): 15–22.
  15. Weisinger HS, Pesudovs K (2002). Optical complications in congenital rubella syndrome. Optometry 73 (7): 418–24.
  16. Freij BJ, South MA, Sever JL (1988). Maternal rubella and the congenital rubella syndrome. Clin Perinatol 15 (2): 247–57.
  17. Reef SE, Frey TK, Theall K, et al. (2002). The changing epidemiology of rubella in the 1990s: on the verge of elimination and new challenges for control and prevention. JAMA 287 (4): 464–72.
  18. Reef S (2006). Rubella mass campaigns. Curr. Top. Microbiol. Immunol. 304: 221–9.
  19. Plotkin SA (2001). Rubella eradication. Vaccine 19 (25-26): 3311–9.
  20. Cooper, L.Z. Congenital Rubella in the United States. 1975 In: Krugman, S Gershon, A (eds), Symposium on Infections Of the Fetus and Newborn Infant. New York, Alan R. Liss Inc.,p.1.
  21. Danovaro-Holliday MC, LeBaron CW, Allensworth C, et al. (2000). A large rubella outbreak with spread from the workplace to the community. JAMA 284 (21): 2733–9.
  22. 22.0 22.1 Ackerknecht, Erwin Heinz (1982). A short history of medicine, 129, Baltimore: Johns Hopkins University Press.
  23. Wesselhoeft C (1949). Rubella and congenital deformities. N. Engl. J. Med. 240 (7): 258–61.
  24. 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
  25. 25.0 25.1 25.2 Lee JY, Bowden DS (2000). Rubella virus replication and links to teratogenicity. Clin. Microbiol. Rev. 13 (4): 571–87.
  26. 26.0 26.1 26.2 26.3 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. URL accessed 2007-07-03.
  27. 27.0 27.1 27.2 27.3 (April 2006) "Chapter 11 - Rubella" Immunisation Handbook 2006, Ministry of Health, Wellington, NZ.. URL accessed 2007-07-03.
  28. Smith, J. L. Contributions to the study of Rötheln. Trans. Int. Med. Congr. Phil. 4,14. 1881
  29. Hess, Alfred Fabian (1914). German measles (rubella): an experimental study. The Archives of Internal Medicine 13: 913–916. as cited by Enersen, Ole Daniel Alfred Fabian Hess. WhoNamedIt. URL accessed on 2007-07-03.
  30. J.B. Hanshaw, J.A. Dudgeon, and W.C. Marshall. Viral diseases of the fetus and newborn. W.B. Saunders Co., Philadelphia, 1985

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