RUBELLA

By Emile K. Nguettia

Rubella infection is commonly known as "German measles" or "3-day measles." The term "German" has nothing to do with the country, but probably came from the Old French term "germain" and the Latin term "germanus," meaning "akin to" or "similar."

The rubella virus passes from person to person through droplets and fluids from the nose and throat, coughing, sneezing, or talking. Persons with rubella are contagious from one week before the rash appears until one week after it fades. [1]

Rubella is caused by the rubella virus, which can be found in the throat, blood, and stool of an infected person. The rubella virus is a member of the Togaviridae, and has been allocated a genus of its own &endash; the Rubivirus. [2] It is roughly spherical with a diameter of 60-70 nm. It has an icosahedral (20-faced) nucleocapsid, which contains the single-stranded RNA genome. This core is surrounded by a lipoprotein envelope, which contains two polypeptides known as E1 and E2. E1, a glycosylated polypeptide which is found on surface projections of the virus, is a hemagglutinin. Only one antigenic type of the virus is known. [3]

A major rubella pandemic that originated in Europe in the early 1960s reached the USA in 1964, causing an estimated 12.5 million cases of the disease. The result of this major outbreak was devastating, with 11,000 miscarriages, stillbirths and terminations, and the birth of 20,000 infants with congenital rubella syndrome (CRS). [ 3]

Due to limited disease surveillance and reporting systems there are insufficient data on rubella in the developing world. Rubella is often not notified as many cases are not seen by a doctor or even recognized by the patient and rubella outbreaks can occur with no clinical recognition. Studies in Central and South America, Africa, India and the Middle and Far East suggest that rubella is widespread and endemic in most developing countries. [3 ] In countries with the highest susceptibility rates (>25%) among women of childbearing age, including Jamaica, Malaysia, Panama, Singapore and Sri Lanka, serological data are consistent with other data showing a high incidence of CRS and/or a high proportion of acquired rubella among pregnant women. [3 ] In other countries with high or moderate susceptibility rates such as Brazil, parts of India, and Nigeria, the absolute risk of CRS is difficult to estimate and there maybe substantial within-country variation. [3]

Approximately 25-50% of rubella infections are subclinical and may go undetected. When symptoms do present, they are usually quite mild. The main symptoms include inflammation of the lymph nodes and a maculopapular rash, which may be preceded by mild catarrhal symptoms. [2] Enlargement of the lymph nodes (lymphadenopathy) occurs from 5-7 days [ ]. Swelling of the lymph nodes is common, as are joint pain and temporary arthritis, the latter particularly in women. [4] These symptoms are not specific to rubella, (for example, similar symptoms can be seen in measles and taxoplasmosis), however, rubella causes considerably greater enlargement of the lymph nodes, which can last for several weeks. [ 2, 4] Mild febrile infectious disease with a diffuse punctuate and macular rash resembling measles; leukopenia; arthralgia and arthritis may arise as complication, especially in adult females; half of infections occur without rash; Congenital rubella syndrome (CRS) may occur in infants born to women with rubella in first trimester &endash; death, spontaneous abortions, congenital malformations, risk decreases with fetal development. [3] If a woman gets rubella in the early month of her pregnancy, her chance of giving birth to a deformed baby may be as high as 80%. These babies may be born deaf or blind. They may have damaged hearts or unusually small brains. Many are mentally retarted. The last big rubella epidemic was in 1964. As a result of that epidemic about 20,000 babies were born with severe birth defects. [1]

The rubella virus multiplies in the lining of the respiratory tract or in local lymph nodes before passing into the bloodstream and spreading throughout the rest of the body. In pregnant women, the blood-borne virus may infect the placenta and replicate there. It can then spread to the fetal circulation. During fetal growth, the rubella virus inhibits the division of a number of different cell types and thus disrupts the development of many organs. In some organs, including the eye, the ear and the brain, infection may interfere with the blood supply, resulting in even more damage. [3]

Vaccination is the best method of preventing rubella. Soon after the rubella virus was first isolated in tissue culture in 1962, several live-attenuated vaccine strains were developed. HPV-77 (duck embryo), HPV-77 (dog kidney) and Cendehill (rabbit kidney) strains were originally licensed in the USA between 1969 and 1970. These vaccines were replaced in 1979 by RA 27/3 (human diploid fibroblast), which produces a strong immune response (similar to natural infection) of 95% or more. While rubella immunity induced by vaccination has been reported to persist for at least 16 years and probably to be lifelong, other recent data indicate that this immunity may wane after 8 years of age. [3] Rubella vaccine is usually offered in combination with measles (MR) or measles and mumps (MMR) vaccines. [1,5] This combination offers the same high levels of immunogenicity and safety as does its individual components. Most of the currently licensed vaccines are based on a live, attenuated strain of rubella virus known as RA 27/3. The vaccines are administered subcutaneously. To avoid interference with possible remaining maternal antibodies the vaccine is usually given at the age of 12-15 months. Attempts to develop killed virus vaccines or sub-component vaccines against rubella have not been successful. [5] A study of persistence of immunity following vaccination with MMR showed that about 97% of vaccinees remained positive up to 15 years after vaccination and vaccine induced protection is generally assumed to be lifelong. Although it is unlikely that the attenuated virus strains used in the current rubella vaccines are harmful to the fetus, pregnant women should not receive the vaccine due to the theoretical, but never demonstrated, risk of CRS to the unborn fetus. However, no brain defects caused by CRS were found in more than 1,000 babies born to susceptible women who were inadvertently vaccinated within 3 months of conception. Persons suffering from advanced immuno-deficiency including congenital immune disorders, malignancies, and immuno-suppressive therapy are also advised against rubella vaccination. However, HIV positive children, when exhibiting no symptoms, and children with leukaemia in stable remission, should be immunized. Patients with a history of extreme sensitivity to the antibiotic neomycin should not receive rubella vaccine. [5] The goal of rubella vaccination is to prevent congenital rubella infection. It can be achieved only by protecting all women of child-bearing age, as well as other people who come in contact with them, such as family members, co-workers, and other contacts. [1] The general WHO requirements for new vaccines are met by the current RA 27/3 based rubella vaccine and its MR or MMR combinations. The World Health Organization recommends the use of rubella vaccine in all countries with well functioning childhood immunization programmes where reduction or elimination of CRS is considered a public health priority, and where appropriate resources may be utilized. [1, 4, 5]

References:

1. "Rubella (German Measles)" from the Centers for Disease Control and Prevention. March 9, 1995. URL:www.babybag.com/articles/cdc_rbla.htm. Visited on 4/28/02.

2. "Rubella Virus". May 12, 1999. URL:

3. "Worldwide Vaccines: Measles &endash; Mumps &endash; Rubella". January 3, 2002. URL: www.worldwidevaccines.com/public/diseas/measlesTOC.asp. Visited on 4/26/02.

4. "Vaccines, Immunization, and Biologicals: rubella". 2001. URL: www.who.int/vaccines/en/rubella.shtml. Visited on 5/01/02.

5. Sander, D. "The Big Picture Book of Viruses &endash; Togaviruses". 1995-2001. http://www.virology.net/Big_Virology/BVRNAtoga.html Visited on 5/01/02.