This article is about the disease. For the virus, see rubella virus.
| Rubella |
| Classification and external resources |
Transmission electron micrograph of rubella virus
|
| ICD-10 |
B06 |
| ICD-9 |
056 |
| DiseasesDB |
11719 |
| MedlinePlus |
001574 |
| eMedicine |
emerg/388 peds/2025 derm/259 |
| MeSH |
D012409 |
Rubella, also known as German measles or three-day measles,[1] is a disease caused by the rubella virus. The name "rubella" is derived from 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.[2]
Rubella is a common childhood infection that can sometimes be fatal usually with minimal systemic upset although transient arthropathy may occur in adults. Serious complications such as deterioration of the skin 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 (can be passed along by the breath of people sick from Rubella). 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.[3] 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.
The name rubella is sometimes confused with rubeola, an alternative name for measles in English-speaking countries; the diseases are unrelated.[4][5] In some other European languages, like Spanish, rubella and rubeola are synonyms, and rubeola is not an alternative name for measles.[6] Thus, in Spanish, "rubeola" refers to rubella and "sarampión" refers to measles.
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Contents
- 1 Signs and symptoms
- 1.1 Congenital rubella syndrome
- 2 Cause
- 3 Diagnosis
- 4 Prevention
- 5 Treatment
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 See also
- 10 References
- 11 External links
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Signs and symptoms[edit]
Rash of rubella on skin of child's back. Distribution is similar to that of measles but the lesions are less intensely red.
After an incubation period of 14–21 days, German measles causes symptoms that are similar to the flu. 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 (that is why it is often referred to as three-day measles). The facial rash usually clears as it spreads to other parts of the body. Other symptoms include low grade fever, swollen glands (sub occipital & posterior cervical lymphadenopathy), joint pains, headache and conjunctivitis.[7]
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 of German measles is typically pink or light red. The rash causes itching and often lasts for about three days. The rash disappears after a few days with no staining or peeling of the skin. When the rash clears up, the skin might shed in very small flakes where the rash covered it. 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 two-thirds 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 patient is contagious typically for about one week before he/she develops a rash and for about one week thereafter.
Congenital rubella syndrome[edit]
Main article: Congenital rubella syndrome
Rubella can cause congenital rubella syndrome in the newly born. The syndrome (CRS) follows intrauterine infection by the Rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects.[8] 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.[9]
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 (Patent ductus arteriosus being the most common), blindness, deafness, or other life threatening organ disorders. The skin manifestations are called "blueberry muffin lesions".[9] For these reasons, Rubella is included on the TORCH complex of perinatal infections.
Cause[edit]
Main article: Rubella virus
The disease is caused by Rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome.[10] 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. The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.[7]
Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are involved in virus infection or non-resolution of the disease.[11] [12]
Diagnosis[edit]
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.[13] The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.[14]
Prevention[edit]
Further information: 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.[citation needed]
The vaccine is now usually 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.[15]
The immunisation 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.[16][17]
Screening for rubella susceptibility by history of vaccination or by serology is recommended in the United States for all women of childbearing age at their first preconception counseling visit to reduce incidence of congenital rubella syndrome (CRS).[18] It is recommended that all susceptible non-pregnant women of childbearing age should be offered rubella vaccination.[18] Due to concerns about possible teratogenicity, use of MMR vaccine is not recommended during pregnancy.[18] Instead, susceptible pregnant women should be vaccinated as soon as possible in the postpartum period.[18]
Treatment[edit]
There is no specific treatment for Rubella; however, 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[citation needed] and cataracts can be corrected by direct surgery.[19]
Management for ocular congenital rubella syndrome (CRS) is similar to that for age-related macular degeneration, including counseling, regular monitoring, and the provision of low vision devices, if required.[20]
Prognosis[edit]
Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.[21]
Epidemiology[edit]
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.[22] Since the introduction of vaccine, occurrences have become rare in those countries with high uptake rates.
Vaccination has interrupted the transmission of rubella in the Americas: no endemic case has been observed since February 2009.[23] Since the virus can always be reintroduced from other continents, the population still need to remain vaccinated to keep the western hemisphere free of rubella. 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.[24][25] Universal immunisation producing a high level of herd immunity is important in the control of epidemics of rubella.[26]
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.[27]
History[edit]
Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740,[28] which was confirmed by de Bergen in 1752 and Orlow in 1758.[29]
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 (contemporary German Röteln), hence the common name of "German measles".[30] Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name "rubella" (from the Latin word, meaning "little red") in 1866.[28][31][32][33]
It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.[34] In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.[35] In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.[32]
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.[31][32] 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.[31][33]
There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.[33] 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 [36][37]
In 1969 a live attenuated virus vaccine was licensed.[32] In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.[33]
See also[edit]
- Eradication of infectious diseases
- Exanthema subitum (roseola infantum)
- List of cutaneous conditions
References[edit]
- ^ Neighbors, M; Tannehill-Jones, R (2010). "Childhood diseases and disorders". Human diseases (3rd ed.). Clifton Park, New York: Delmar, Cengage Learning. pp. 457–79. ISBN 978-1-4354-2751-8.
- ^ 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. PMID 5581012.
- ^ 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. doi:10.1097/00006454-200104000-00004. PMID 11332662.
- ^ Merriam-webster:Rubeola Accessed 2009-09-20.
- ^ T. E. C. Jr. Letters to the editor Pediatrics Vol. 49 No. 1 January 1972, pp. 150-151.
- ^ Webster's Online Dictionary: German measles Accessed 2009-09-20
- ^ a b 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. doi:10.1615/JLongTermEffMedImplants.v15.i3.80. PMID 16022642.
- ^ 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. doi:10.1002/bdra.20045. PMID 15259032.
- ^ a b De Santis M, Cavaliere AF, Straface G, Caruso A (2006). "Rubella infection in pregnancy". Reprod. Toxicol. 21 (4): 390–8. doi:10.1016/j.reprotox.2005.01.014. PMID 16580940.
- ^ Frey TK (1994). "Molecular biology of rubella virus". Adv. Virus Res. 44: 69–160. doi:10.1016/S0065-3527(08)60328-0. PMID 7817880.
- ^ 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. PMID 12463994.
- ^ 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. doi:10.1111/j.1399-0039.1975.tb00520.x. PMID 1138435.
- ^ Best JM (2007). "Rubella". Semin Fetal Neonatal Med 12 (3): 182–92. doi:10.1016/j.siny.2007.01.017. PMID 17337363.
- ^ 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. PMID 12150751.
- ^ 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. PMID 9639369.
- ^ 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 (Supplement 3): S158–63. doi:10.1086/505949. PMID 16998776.
- ^ Centers for Disease Control and Prevention (CDC) (2005). "Elimination of rubella and congenital rubella syndrome--United States, 1969-2004". MMWR Morb. Mortal. Wkly. Rep. 54 (11): 279–82. PMID 15788995.
- ^ a b c d Health Care Guideline: Routine Prenatal Care. Fourteenth Edition. By the Institute for Clinical Systems Improvement July 2010.
- ^ 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. doi:10.4103/0019-5359.29593. PMID 17197734.
- ^ Weisinger HS, Pesudovs K (2002). "Optical complications in congenital rubella syndrome". Optometry 73 (7): 418–24. PMID 12365660.
- ^ Freij BJ, South MA, Sever JL (1988). "Maternal rubella and the congenital rubella syndrome". Clin Perinatol 15 (2): 247–57. PMID 3288422.
- ^ 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. doi:10.1001/jama.287.4.464. PMID 11798368.
- ^ [1] Accessed 2010-04-10.
- ^ Plotkin SA (2001). "Rubella eradication". Vaccine 19 (25-26): 3311–9. doi:10.1016/S0264-410X(01)00073-1. PMID 11348695.
- ^ 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.
- ^ 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. doi:10.1001/jama.284.21.2733. PMID 11105178.
- ^ Reef S (2006). "Rubella mass campaigns". Curr. Top. Microbiol. Immunol. 304: 221–9. doi:10.1007/3-540-36583-4_12. PMID 16989272.
- ^ a b Ackerknecht, Erwin Heinz (1982). A short history of medicine. Baltimore: Johns Hopkins University Press. p. 129. ISBN 0-8018-2726-4.
- ^ Wesselhoeft C (1949). "Rubella and congenital deformities". N. Engl. J. Med. 240 (7): 258–61. doi:10.1056/NEJM194902172400706. PMID 18109609.
- ^ 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
- ^ a b c Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clin. Microbiol. Rev. 13 (4): 571–87. doi:10.1128/CMR.13.4.571-587.2000. PMC 88950. PMID 11023958.
- ^ a b c d 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.
- ^ a b c d "Chapter 11 - Rubella". Immunisation Handbook 2006. Ministry of Health, Wellington, NZ. April 2006. ISBN 0-478-29926-5. Retrieved 2007-07-03.
- ^ Smith, J. L. Contributions to the study of Rötheln. Trans. Int. Med. Congr. Phil. 4,14. 1881
- ^ 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.
- ^ J.B. Hanshaw, J.A. Dudgeon, and W.C. Marshall. Viral diseases of the fetus and newborn. W.B. Saunders Co., Philadelphia, 1985
- ^ "EPI Newsletter Volume XX, Number 4". Pan American Health Organization. August 1998. Retrieved 2007-07-03.
External links[edit]
- Rubella at Wong's Virology.
- Immunization Action Coalition: Rubella
- Rubella risks during different periods of pregnancy
- DermNet viral/rubella
- Centers for Disease Control and Prevention (2012). "Ch. 19: Rubella". In Atkinson W, Wolfe S, Hamborsky J. Epidemiology and Prevention of Vaccine-Preventable Diseases (12th ed.). Washington DC: Public Health Foundation. pp. 275–290.
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Infectious skin disease: Viral cutaneous conditions, including viral exanthema (B00–B09, 050–059)
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DNA virus
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Herpesviridae
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Alpha
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HSV (Herpes simplex, Herpetic whitlow, Herpes gladiatorum, Herpetic keratoconjunctivitis, Herpetic sycosis, Neonatal herpes simplex, Herpes genitalis, Herpes labialis, Eczema herpeticum, Herpetiform esophagitis) · Herpes B virus (B virus infection)
VZV (Chickenpox, Herpes zoster, Herpes zoster oticus, Ophthalmic zoster, Disseminated herpes zoster, Zoster-associated pain, Inflammatory skin lesions following zoster infection, Modified varicella-like syndrome)
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Beta
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Human herpesvirus 6/Roseolovirus (Exanthema subitum, Roseola vaccinia)
Cytomegalic inclusion disease
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Gamma
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KSHV (Kaposi's sarcoma)
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Poxviridae
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Ortho
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Variola (Smallpox, Alastrim) · MoxV (Monkeypox) · CV (Cowpox) · VV (Vaccinia, Generalized vaccinia, Eczema vaccinatum, Progressive vaccinia)
Buffalopox
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Para
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Farmyard pox: Milker's nodule · Bovine papular stomatitis · Pseudocowpox · Orf
Sealpox
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Other
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Yatapoxvirus: Tanapox · Yaba monkey tumor virus
MCV (Molluscum contagiosum)
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Papillomaviridae
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HPV (Wart/Plantar wart, Heck's disease, Genital wart (giant), Laryngeal papillomatosis, Butcher's wart, Bowenoid papulosis, Epidermodysplasia verruciformis, Verruca plana, Pigmented wart, Verrucae palmares et plantares )
BPV (Equine sarcoid)
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Parvoviridae
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Parvovirus B19 (Erythema infectiosum, Reticulocytopenia, Papular purpuric gloves and socks syndrome)
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Polyomaviridae
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Merkel Cell Polyomavirus (Merkel Cell carcinoma)
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RNA virus
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Paramyxoviridae
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MeV (Measles)
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Togaviridae
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Rubella virus (Rubella, Congenital rubella syndrome) · Alphavirus infection · Chikungunya fever
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Picornaviridae
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CAV (Hand, foot and mouth disease, Herpangina) · FMDV (Foot-and-mouth disease) · Boston exanthem disease
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| Ungrouped |
unknown/multiple: Asymmetric periflexural exanthem of childhood · Post-vaccination follicular eruption · Lipschütz ulcer · Eruptive pseudoangiomatosis · Viral-associated trichodysplasia · Gianotti–Crosti syndrome
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cutn/syst (hppv/hiva, infl/zost/zoon)/epon
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drug (dnaa, rnaa, rtva, vacc)
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noco (i/b/d/q/u/r/p/m/k/v/f)/cong/tumr (n/e/d), sysi/epon
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proc, drug (D2/3/4/5/8/11)
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