Rubella

 

Rubella. (German Measles)

 

Part One: The disease.

Internet URLs: http://pathmicro.med.sc.edu/mhunt/rubella.htm

http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.figgrp.2966

CDC power point 

Compilation from various older medical text books I have.

(I prefer these, because they are written by practical people who have seen the diseases many times, and can accurately describe the symptom variations.)

Rubella virus was isolated from cell cultures of throat swabbings from infected people, in 1962 at America’s Harvard University and independently at Walter Reed Army Institute of Research. The virus is a moderately large single-stranded RNA virus 50 to 70 nm in diameter classified as Rubivrinae, but has similarities to the family Togavirus, and its laboratory behaviour is very 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 has been found in throats, blood and faeces for up to 7 days before any rash is seen, and in throat washings up to 2 weeks after onset.

Pathogenesis:

Rubella is not as contagious as measles nor does it have the potential for sequalae in children. It is frequently confused with other infections with rash, and even in 1977 (Harrisons) it was stated that, “A certain diagnosis of rubella can be made only by virus isolation and identification, or by changes in antibodies titres.”

Severity varies from subclinical to mild. The virus affects humans exclusively, in whom it causes two disease presentations: a benign exanthem (blotchy 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.

Congenital infections:

Effects of rubella infectious during the first trimester of rubella infections were first reported by Sir Norman Gree after a rubella in Australia in 1940.

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, because that doesn’t appear to have been studied.

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. The only decent study I could find looking at the issue properly was this one which showed this chart.

Therefore the question needs to be asked: What has eliminated congenital rubella – routine abortion or the use of the rubella vaccine?

Delayed effects of congenital rubella but I've not seen this information in any other text I've looked at.

Rubella Infection : clinical course.

Incubation time (from exposure to start of rash) is 14 – 21 days, usually about 18 days, according to Harrison’s. Harrison’s “Principles of Internal Medicine” also says, “It is apparent from serological studies that rubella infection may be associated with no signs or symptoms, or may result in lymph node enlargement without skins lesions…respiratory symptoms may be mild or absent. Small red lesions (Forchheimer’s spots) may be see on the soft palate but are not pathognomonic of the disease” . 

Other texts say that viraemia occurs in the blood within 7 – 10 days of exposure. 

And USA CDC says 5 – 7 days. Who is right? Who knows?

The textbook, Pathology of Infectious Diseases, says that the first symptom in young children is the appearance of a rash usually beginning on the forehead and face and spreading downwards. The rash is a lighter hue than measles, very small, almost like a heat rash, and they can coalesce to form a blotchy rash similar to scarlet fever. The rash is usually there for around 3 days, but anywhere from 1 to 5 is normal.

In my experience, except in very, very mild cases, parents who say a rash comes first may not have noticed 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, and swollen glands, which is one symptom that does come before the rash. Rubella usually causes quite distinctive swollen glands, but again, you need to be alert.

The first sign that alerted me to the fact that I had rubella (despite high levels of antibodies) was not the appearance of a rash spreading from my face and neck down my body (which could have been anything), but swollen glands at the back of the neck on both sides and behind the ears in the hollow parts either side of the spine.

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. They can be quite prominent, and can stick around until after the rash has gone.

Text books often say 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.

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, with reports of arthralgias and slight joint swellings, particularly in children or young women, most marked during the period of rash, and 1 – 14 days after all other symptoms have gone.

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 natural rubella experience achy joints with the small joints of the hand and wrist most commonly involved, and about 15% experience arthritis-like symptoms. Women in particular are affected.

In general, the arthritic syndrome lasts about ten days, Carpal tunnel syndrome sometimes accompanies rubella. In rare cases, recurrent joint symptoms can persist.

Very very rarely, encephalomyelitis can occur after rubella, but that is much less common than after measles. Textbooks today also list infrequent complications such as Guillain-Barré and thrombocytopenia.

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). By 1998 it was supposedly 1/6,000 (Krugman, 1998) and by 2003 that had dropped to 1/5,000 (“Clinical Neurovirology” By Avindra Nath, Joseph R. Berger Contributor Avindra Nath, Joseph R. Berger, 2003,ISBN 0824740815) .

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”.

Laboratory detection of blood immunity:
 
Blood test looking for IgG for past infection, and IgM for immediate infection.

Laboratory detection for memory immunity in the absence of detectable antibodies.

There is not test for memory immunity. The absence of detectable antibodies does not mean the absence of actual immunity.

Laboratory detection of presence of virus:

In some countries, rubella is detected using throat secretions, or tissue from the mother or embryo in case of a miscarried baby suspected to be due to rubella. Culture is usually primary monkey cells or human embryonic cells or cell cultures. The tests used are haemagglutination inhibition and complement fixation. Other countries use the PCR (Polymerase chain reaction ), or other NAT tests (Nucleic Acid Testing) 

Diagnostic medlab handbook (depending on who gets the contract next year, this handbook may disappear)

Epidemiology.

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.)

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”?

Differential Diagnoses:

Rubella is usually carefully considered and compared with scarlet fever and English measles, because, depending on the severity, the symptoms can appear similar.

Clinical specifics:

Soft palate spots vary with the disease with rubella showing pinpoint red spots on the soft palate; scarlet fever shows raised red spots, and English measles, Koplik’s spots which are red, with white “salt-grain middles”.

The rash of English measles leaves behind a brownish stain on the skin for a few days, whereas rubella rash comes and goes with no difference on the skin. If you’re dealing with mild symptoms which could be either measles or rubella, this browning, or lack of, might clinch the diagnosis. This increased browning, or pigmentation, is quite specific to English measles. (Ped. Inf. Dis. 1997). Most of the clinical symptoms are gone by five days.

Some references

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.
12. Harrison’s Principles of Internal Medicine, 1977.

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