Review Of The viral disease Of Pediatric importance (Rubella

This paper gives a review of the rubella virus, one of the most important viruses of pediatric importance. It delves into the epidemiological patterns .It also highlights the peculiarities of the clinical features using well researched available data, the fate of the child caught in the web of this benign but potentially fatal and handicapping disease. It finally concludes by prognosticating and predicting the future possible exploration on the virus.

Background

     Rubella is caused by specific virus which can be detected in both blood and nasopharyngeal secretions during the acute stage of the disease  it is an RNA virus usually spherical in shape and can now be grown in a variety of tissue culture and the various strain belong to one serological type. Haemaglutination and complement fixing antigens have been prepared and the inhibition of these by specific anti-sera has formed the basis for practical serological test. Rubella (also known as German measles) is a common contagious disease caused by a virus. Most cases of it are not serious. However, if a woman catches it during early pregnancy, it may result a number of birth defects. The virus causing Rubella is an airborne virus. This makes the virus extremely contagious. Two or three weeks after contact with the virus, a person may develop several symptoms. These include a runny nose, sore throat, and mild fever. Pink, slightly raised spots may appear on the body. Rubella virus is the sole member of the family Togaviridae with characteristic positive single stranded RNA covered with icosahedra capsid.The genome of the virus encoding measures up to 9757 nucleotide and is responsible for the encoding of 3 structural and 3 non structural protein (Dominninnez, Wang&Frey 1990).Capsid protein are found in the cytoplasm where they interact with genomic RNA to form capsid (Garbutt etal 1999).Another small sub genomic RNA is embedded in a virion (Togaviridae). The synthesis of the capsid takes place at the surface of the intracellular membrane at the same time with the budding of the virus (Beatch &Hobman 2000).

Epidemiology

Rubella is universally. More incidence of the disease is common in spring in nations with temperate climate. Prior to the discovery of Rubella vaccine in 1969, outbreak is noted every 4 year in Europe and every 7 year in US with most affectation in children between 5 to 7 years of age. High incidence has decreased with the discovery of the vaccine however large number of cases of unvaccinated men are still found in the UK.Majority of the pregnant women infected got the virus in the 1993 and 1996 outbreak in UK and they were immigrants.Inaccebility and the high cost of the vaccine still make outbreak inevitable in the developing countries (Richardson etal 2001).Congenital rubella syndrome is responsible for an estimated 30000 fresh stillbirth and 20000 congenitally born children with rubella in 1962 to 1965 epidemics in the US (Siegel, Fuerst &Guinee 1971).For epidemics to be well controlled, there will be need for global immunization. This will result in herd immunity against the virus (Watson etal 1998)

Clinical features

     The incubation period of rubella is approximately 10-18 days in children the first symptom is the development of rash over the face in adolescent however fever malaise and headache are frequent early complaints .The rash rapidly spread to involve the neck trunk and extremity so that by the end of first day of the illness the entire body may be covered with pinkish discrete maculesAt times the macules coalesce on the trunk but not on the limbs They rapidly fade so that in the typical case the rash has diapered by the end of the third da.The rash  of rubella is far from specific and an identical rash may be seen in many other viral infections. A similar rash may also be present in glandular fever, in serum sickness, in other allergic states and following drug ingestion. Generalized lymphadenopathy is a feature of typical rubella although on rare occasions it may be absent. The nodes particularly involved are the suboccipital, post auricular and the cervical. These nodes may be slightly tender for a day or so Fever is usually of mild degree merely rising above 38 degress in children and rarely longer than one day. Rubella in childhood is a benign illness and recovery without complications is the rule in adolescent a polyarthitis lasting a week to 10 days not infrequently appears on about the third day. Encephalitis and thrombocytopenia purpura are extremely rare complications. The risk of Rubella infection from an infected mother is high and when this happens in early pregnancy it causes severe disturbance in embryogenesis with severe consequences. Congenital rubella syndrome (CRS) can occur in a developing fetus of a pregnant woman who has contracted rubella during her first trimester. Problems rarely occur when rubella is contracted by the mother after 20 weeks of gestation. The classical triad of congenital rubella syndrome is cataract, congenital heart diseases and deafness. Other features include low birth weight, with other heart lesions(microphthalmia,retinopathy),central nervous system lesions(microcephaly and meninigoencephalitis),hepatosplenomegaly,jaundice,thrombocytopenia(Edlich etal 2005).The  basis for the congenital rubella syndrome is not well understood however studies reveal the apoptotic  effect of the virus over some cells and also proof of a P53 dependent mechanism(Megyeri etal 1999).  It was discovered in 1941 by Australian Norman McAllister Gregg (1892-1966).The common cardiac defects are patent ductus arterisus, ventricular septal defects and tetra logy of fallot.The affected children may show features of multiple congenital malformations or only one feature such as cataract or glaucoma.

Diagnosis

This is suggestive from the clinical pattern but it may be confused with the rash of a number of other viral illnesses and with drug eruption .Confirmation of a suspected case is essential in pregnant women or her contacts .Although the virus can usually be isolated from the pharynx within 5 days after the onset of the rash these facilities are generally unavailable so that serology tests may be required. For this, the initial specimen should be obtained as early as possible and the convalescent specimen 2-4 weeks later. A fourfold or greater rise in titer indicates a recent infection. The haemaglutination inhibition test is most generally used. Antibodies to rubella may also be detected by specific neutralization and complement fixation tests. 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 (Best 2007). Diagnosis may be obvious at birth but viral studies where possible should be done. In the acute phase the virus may be isolated from the nasopharyngeal washing or blood. IgM specific antibody may remain positive long after the infection.Severly affected infants may continue to excrete the virus after birth and infect susceptible contacts.

Treatment

As rubella is a benign disease treatment is unnecessary. There is no specific treatment for the affected infants but supportive and rehabilitative care should be applied at all times. Congenital heart defects and cataracts can be corrected by surgery (Khandekan etal 2007)

Prevention and prognosis

Prevention is possible through immunization of girls with the rubella vaccine .This is now routine In most countries. A live vaccine is now available for the prevention of rubella. It is safe and effective but still expensive .For those countries able to afford the vaccines, it is recommended that all females should be given before puberty .It is also recommended that married females be screened by the H.I test and immunized if antibodies are not detected. Under no circumstances should the vaccine be administered if there is possibility of pregnancy. The recommended time for immunization is immediately after parturition. Prognosis is poor in newborn with congenital rubella syndrome (Seagel etal 1971).

References

Best JM (2007). “Rubella”. Semin Fetal Neonatal Med 12 (3): 182–92. doi: 10.1016/j.siny.2007.01.01

Dominguez G, Wang CY, Frey TK (July 1990). “Sequence of the genome RNA of rubella virus: evidence for genetic rearrangement during togavirus evolution”. Virology 177 (1): 225–38. PMID 2353453.

Megyeri K, Berencsi K, Halazonetis TD, et al (June 1999). “Involvement of a p53-dependent pathway in rubella virus-induced apoptosis”. Virology 259 (1): 74–84. doi:10.1006/viro.1999.9757. PMID 10364491.

Bardeletti G, Kessler N, Aymard-Henry M (1975). “Morphology, biochemical analysis and neuraminidase activity of rubella virus”. Arch. Virol. 49 (2-3): 175–86. PMID 1212096.

 “Togaviridae- Classification and Taxonomy”. http://www.stanford.edu/group/virus/toga/class.html.

 Garbutt M, Law LM, Chan H, Hobman TC (May 1999). “Role of rubella virus glycoprotein domains in assembly of virus-like particles”. J. Virol. 73 (5): 3524–33. PMID 10196241. PMC: 104124. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=10196241.

 Beatch MD, Everitt JC, Law LJ, Hobman TC (August 2005). “Interactions between rubella virus capsid and host protein p32 are important for virus replication”. J. Virol. 79 (16): 10807–20. doi:10.1128/JVI.79.16.10807-10820.2005. PMID 16051872.

 Beatch MD, Hobman TC (June 2000). “Rubella virus capsid associates with host cell protein p32 and localizes to mitochondria”. J. Virol. 74 (12): 5569–76. PMID 10823864. PMC: 112044. http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=10823864.

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C.M. Fauquet, M.A. Mayo et al.: Eighth Report of the International Committee on Taxonomy of Viruses, London San Diego 2005.

 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.

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

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

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