[back] Rubella


By Hilary Butler

Rubella virus is a moderately large single-stranded RNA virus classified in the family Togavirus, although its laboratory behaviour is more like that of the paramyxoviruses. Rubella virus is highly sensitive to heat, to extremes of pH and to a variety of chemical agents. The virus affects humans exclusively, in whom it causes two disease presentations: a benign exanthem (rash) in children 5 to 9 years old (pre-vaccine era), and a potentially devastating congenital infection if a pregnant woman has clinical symptoms in the first three months of pregnancy.

Rubella outbreaks usually occur during the spring months in temperate zones such as New Zealand. Before vaccination campaigns, rubella tended to appear in epidemics of 3 – 4 year cycles at 6 – 9 year intervals and 80-90% of adults were immune (MOH, 1996). Since vaccination campaigns started, however, the typical age range of 5 to 9 years is no longer applicable and rubella can affect any age group. Within 4 years of widespread vaccine use in the United States, medical literature was reporting that:

"There appears to have been a slight upward shift in the age-specific incidence of rubella." (Paediatrics, vol. 55 no. 1 Jan 1975.)

The current assessment of risk of congenital malformations after rubella infection in pregnancy is confusing. On the one hand, Krugman (p. 412) says:

"30 – 50% during the first four weeks of gestation. 25% in the fifth to eighth week; 8% in the ninth to twelfth week. A slight risk of deafness during the thirteenth to sixteenth week. Overall risk of malformations in the first trimester is approximately 20%."

And on the other hand, Carlos Abramowsky (1997) states:

 "The probability of having a congenital defect ranges from 90% for infection in the first trimester to 25% for infection in the second trimester."

Rather a discrepancy – and don’t ask me who’s right!

If you are told that your baby’s congenital defects are caused by rubella, don’t accept this diagnosis without extensive blood work to prove it. Some doctors think TORCH defects (the acronym for Toxoplasmosis, Other viruses, Rubella, Cytomegalovirus and Herpes Simplex) can only be caused by rubella, but as the acronym states, a raft of other viruses can also cause many of the same defects.

Research on the pathogenesis of defects has centred on inhibition of cell division and an increased number of chromosome breaks. While medical people can tell you what happens, they have no idea how it happens, or what the role of maternal nutrition is in this process.

The medical literature states that the introduction of the rubella vaccination has resulted in the virtual elimination of congenital rubella. This "opinion" ignores the fact that since the last major outbreak in 1965, routine abortion was, and is, offered to all women who acquire rubella when they are pregnant. Most women accept.

To say that all congenital rubella cases have been eliminated by vaccination ignores the fact that abortions routinely offered to women exposed to rubella also eliminate all those babies who would not have had congenital abnormalities. Therefore the question needs to be asked: What has eliminated congenital rubella – routine abortion or the use of the rubella vaccine?

Clinical symptoms and complications of rubella

The first symptoms of rubella occur after an incubation period of approximately 16 to 18 days, with a range of 14 to 21 days.

The textbook, Pathology of Infectious Diseases, says that the first symptom in young children is the appearance of a rash. In my experience, except in very, very mild cases, parents who echo this may not be noticing the moods and health of their young ones. In both our children, there were two days of a low fever, whinging, disinterest in life in general, and rubbing of eyes.

The same textbook says that adolescents and adults will experience low grade fever, headache, malaise, anorexia, mild conjunctivitis, coryza, sore throat, cough and lymphadenopathy, and that these symptoms rapidly subside after the first day of rash.

At one time, textbooks stated that there were no rare complications:

"Complications and sequelae are for all practical purposes non-existent." (Box, 1937).

By 1940, it became obvious that this was no longer the case and the possibility that the virus had changed and become ‘neurotropic’ was considered. (BMJ, August 3, 1940, p. 154.) Whether this was so is hard to determine, but it does seem that references to more extensive and serious arthritis following rubella in children and post-pubertal females became far more common.

Textbooks today list infrequent complications such as arthritis in multiple joints, encephalitis, Guillain-Barré and thrombocytopenia.

Arthritis in younger children is characterised primarily by involvement of the knees and difficulty getting up and walking. It is known as 'catcher’s crouch’ (since children get ‘caught’ in the position adopted by cricket fielders in the slip cordon). The majority of adults contracting rubella experience sore joints, and about 15% experience arthritis-like symptoms. Women in particular are affected. In general, the arthritic syndrome lasts about ten days, with the small joints of the hand and wrist most commonly involved. Carpal tunnel syndrome sometimes accompanies rubella.

It is interesting to note the changes in ‘incidence’ of these complications over the years. In 1980, the incidence of encephalitis was 1/100,000 clinical severe cases (NZ Med. J. August 13, 1980, p. 104), by 1985 it had climbed to 1/50,000 (J. Inf. 1985, p. 240), in 1989 it was 1/20,000 (NZ Med. J. 26 April 1989, p. 202). Now it is supposedly 1/6,000 (Krugman, 1998).

As with measles and mumps, the risk statistics of each era seem to alter to suit the medical opinion of the moment, dependant on whether there is a perceived need to further promote a "fix-it".

In 1990, there was a rubella outbreak in Auckland with 5 children hospitalised with rubella encephalitis. One of these children died and another had severe residual neurological impairment (NZ Med. J. 26 September 1990, p. 464). The interesting thing about this article is that four of the five children were boys 5 – 11 years, and that there is no discussion regarding socio-economic status or other risk factors. It might seem that rubella encephalopathy is on the increase – or could it be that the poverty problem that has plagued Auckland for decades is marching on, while the medical people’s response, as usual, centres on vigorous promotion of a politically correct and popular "fly-swat"?

Rubella is usually carefully considered and compared with scarlet fever and English measles, because, depending on the severity, the symptoms can appear similar. In rubella, there can be pinpoint red spots on the soft palate. In scarlet fever, the soft palate may be covered with raised red spots. There have also been cases with Koplik’s spots, which are normally associated with English measles. These are red spots inside the cheeks with what look like raised, largish grains of salt sitting on top.

Rubella usually causes quite distinctive swollen glands, but again, you need to be alert. The first sign that alerted me to the fact that, despite antibodies, the ‘problem’ I had during pregnancy could be rubella was not the appearance of a rash spreading from my face and neck down my body (which could have been anything). It was the swollen glands at the back of the neck on both sides and behind the ears. Keep a close eye on these areas and especially discomfort when you touch the back of the neck. Swollen glands without the rash are quite common and you need to be aware of which glands are swollen.

The rash of English measles leaves behind a brownish stain on the skin for a few days, whereas rubella comes and goes with no difference on the skin. If you’re dealing with mild symptoms which could be either, this browning, or lack of, might clinch the diagnosis. Despite the ignorance of many doctors, this browning, or increased pigmentation, is quite specific to English measles. (Ped. Inf. Dis. 1997). Most of the clinical symptoms are gone by five days. Don’t tolerate being told you are imagining things.


  1. Abramowsky, Carlos. 1997. Pathology of Infectious Diseases. Vol. 1. P. 306.
  2. Box, Dr., 1937. Textbook of the practice of medicine. Price. 1937.
  3. British Medical Journal. August 3, 1940. P. 154.
  4. Journal of Infection. Vol. 11, 1985. P. 240.
  5. Krugman. 1997. Infectious diseases of children. 10th edition. 1998.
  6. Ministry of Health. 1996. Immunisation handbook.
  7. New Zealand Medical Journal. August 13, 1980. P. 104.
  8. New Zealand Medical Journal. 26 April 1989. P. 202.
  9. New Zealand Medical Journal. 26 September 1990. P. 464.
  10. Pediatric Infectious Diseases. Vol. 16. No. 9. Sept. 1997. P. 908.
  11. Pediatrics. Vol. 55 No. 1, January 1975.

 [Vaccination]  [Hilary Butler]