Rubella is a directly transmitted immunizing infection that usually occurs during childhood and is associated with low morbidity and mortality. Infection of women during early pregnancy can lead to spontaneous abortion, fetal death or children born with congenital rubella syndrome (CRS), which is associated with multiple disabilities that can require lifelong care , including hearing impairment, cataracts and congenital heart disease

1. University of Baghdad
college of medicine
German measles (Rubella)
CLS-Pathology
Ali Hussein Ahmed
Second grade
Student selected components
2017/2018

2. 2
Contents:
1. Introduction …………………………..……………………………………… 3
2. Search board and discussion:
 Epidemiology ……………………………………………………………. 4
 Signs and symptoms ………………………...…………………………… 6
 Causes ……………………………………...…………………………….. 7
 Laboratory diagnosis ………………………..…………………………… 7
 Vaccine ……………………………………...…………………..……….. 8
 Treatment ……………………………………..…………………………. 9
 History …………………………………………..…………………..….. 10
 Prevention …………………………………………..………………..…. 11
 Etymology …………………………………………………………….... 12
3. summary …………………………………………….……………………… 12
4. References …………………………………………….……………………. 13

3. 3
 INTRODUCTION:
Rubella is a directly transmitted immunizing infection that usually occurs
during childhood and is associated with low morbidity and mortality. Infection of
women during early pregnancy can lead to spontaneous abortion, fetal death or
children born with congenital rubella syndrome (CRS), which is associated with
multiple disabilities that can require lifelong care [1], including hearing
impairment, cataracts and congenital heart disease. [2]
A relatively inexpensive, high efficacy vaccine that provides lifelong
immunity to rubella and can easily be combined as measles–rubella (MR), or
measles–mumps–rubella (MMR) has been available for 50 years. Although
routine rubella vaccination can prevent CRS, inadequate vaccination coverage
may actually increase CRS cases by increasing the average age of infection [3];
this occurs because vaccination short of the threshold required for elimination
effectively reduces incidence in the population, thus reducing the risk of infection
and delaying time to the first infection (figure 1). Consequently, introduction of
rubella-containing vaccine (RCV) has been limited globally. Recent efforts for the
control and elimination of measles have spurred renewed interest in the potential
for rubella control, because the two vaccines are easily combined, and overall
measles vaccination coverage levels have been climbing [4]. In addition, the
Global Alliance for Vaccines Initiative (GAVI) has recently opened a funding
window for rubella vaccination [5]. Madagascar is one of the countries that has
successfully applied for this funding.

4. 4
Fig(1). Theoretical expectations for RCV coverage and the burden of CRS. In a classic SIR
framework, the dynamics of susceptibles are captured by dS/dt = μ(1 − v) − βSI − μS; and infected
by dI/dt = βSI − gI − μI; where μ is the birth and death rate, total population size as taken as N = 1,
v is vaccination coverage of the birth cohort, g is the generation time of the infection and the
transmission rate is β = R0(g + μ). To capture rubella dynamics, we set g to 18 days−1, R0 = 5,
and chose μ = 30 per 1000 per year. (a) The equilibrium proportion of infected individuals I* (y-
axis) is defined by I* = μ[(1 − v)R0 − 1]/β and thus declines with increasing vaccination coverage
(x-axis). (b) Conversely, the average age of infection A (y-axis) increases, following R0 = G/A,
where G is the inverse of the unvaccinated birth rate, G = 1/[μ(1 − v)]. (c) This conjunction of
declining incidence but increasing average age of infection has the potential to yield a situation
where more cases are occurring in women of childbearing age, even though the total number of
cases is declining. As a result, the ratio of the equilibrium burden of CRS in the presence of
vaccination relative to the equilibrium burden of CRS if no vaccination has occurred (y-axis) may
first increase with vaccination coverage relative to the scenario of no vaccination (indicated by the
horizontal grey line); eventually declining when incidence is sufficiently low to offset the increase
in the average age of infection. (Results in the last panel are hypothetical; exact values will depend
on the variance and skew of the distribution of age of infection; as well as pattern of fertility over
age). This pattern of increasing CRS burden with increasing vaccination coverage has been called
‘the paradoxical increase of rubella’.
 Epidemiology:
Under-reporting in the incidence data affected our ability to estimate the
proportion of the population susceptible to rubella (see figure 2a and the electronic
supplementary material, S1). However, the TSIR model indicated a clear pattern
of seasonality in transmission, with low transmission in February, June and
October, which was robust to the range of assumptions about starting proportion
susceptible. Surprisingly, the timing of low transmission does not align with
summer school holidays, in contrast to what has been reported for rubella and
other immunizing childhood infections in many other parts of the world.[6][7][8]
Given low reported incidence, we focused our initial descriptive analysis of the
epidemiology of rubella in Madagascar at the largest administrative scale
available, the six provinces of Madagascar. The average age of infection of rubella
is slightly variable across these provinces, ranging from 6.4 years in the province
of Antananarivo to 8.8 years in Antsiranana. Average age broadly negatively
correlates with province population size (Pearson's correlation between log
population size and average age of infection yields ρ = −0.82, n = 6, p < 0.05),
suggesting an underlying biological driver for this pattern. Two possible drivers of
this average infection age distribution include (i) extinction–recolonization
dynamics, which drive up the average age of infection in smaller population
provinces [9]—implying that provinces with smaller populations also have

5. 5
smaller focal population centres, precluding persistence of rubella or (ii) a higher
R0 for rubella in provinces with larger populations (although see [8] for evidence
that measles, a similar directly transmitted infections, shows no signature of
density-dependent transmission). With the data available, it is not possible to
distinguish between these two possibilities. Using the approximation R0 = G/A
(which assumes negligible stochastic dynamics), where G is the inverse of the
birth rate, and A is the average age of infection, the average age of infection in the
data yields estimates of R0 between 3.9 in Antsiranana province and 5.5 in
Antananarivo province. This range is broadly in line with values previously
reported for this infection.[10][11][12]
Fig(2). The epidemiology of rubella in Madagascar. (a) Reported number of cases through time for
the entire country; (b) associated estimates of transmission from the TSIR model; (c) age
distribution of infection, and average age of infection (vertical lines) associated with each of the
six provinces and (d) Map of incidence in regions of Madagascar across the country with colours
showing incidence per 1000 inhabitants

6. 6
 Signs and symptoms:
Rubella has symptoms that are similar to those of flu. However, 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 and posterior cervical lymphadenopathy), joint
pains, headache, and conjunctivitis.[13]
The swollen glands or lymph nodes can persist for up to a week and the fever
rarely rises above 38 °C (100.4 °F). 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.[14]
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 60% of older girls or women experience joint
pain or arthritic type symptoms with rubella.[15]
In children rubella normally causes symptoms which last two days and
include:[16]
 Rash beginning on the face which spreads to the rest of the body.
 Low fever of less than 38.3 °C (101 °F.)
 Posterior cervical lymphadenopathy.[17]
In older children and adults additional symptoms may be
present including:
 Swollen glands
 Coryza (cold-like symptoms)
 Aching joints (especially in young women)
Rare problems can occur including the following:
 Brain inflammation
Fig 3

7. 7
 Ear infection [18]
Coryza in rubella may convert to pneumonia, either direct viral pneumonia or
secondary bacterial pneumonia, and bronchitis (either viral bronchitis or
secondary bacterial bronchitis).[19]
 Causes:
The disease is caused by rubella virus, a togavirus that is enveloped and has a
single-stranded RNA genome.[20] 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.[21] 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.
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.[22]
 Laboratory Diagnostics:
Clinical specimens for the diagnosis of rubella by virus detection usually
consist of throat swabs (TS), oral fluids (OF) or nasopharyngeal secretions,
and by antibody detection are usually sera or OF.[23] The virus has also been
found in other specimens, including cataract tissue and urine. Urine and TSs or
OFs are about equivalent as sources of viral RNA, but the ease of obtaining
TSs or OFs make these specimens the primary ones that are collected.[24]
Urine is often a source of infectious virus from CRS patients. Specimens for
virus detection and for IgM/IgG detection can be transported by standard
methods.

8. 8
The timing of specimen collection is
important in postnatal rubella. Rubella
virus-specific IgM is present in sera in
only about 50% of rubella cases on the
day of rash, but, at five days after rash,
most rubella cases have detectable
rubella-specific IgM. Most rubella cases
are virus positive on the day of rash and
may be positive from seven to ten days
post rash.[25] Since postnatal rubella is a mild disease of short duration, special
effort is required to obtain samples on the day of rash or shortly thereafter.
Patients with CRS and congenital rubella infection (CRI) are IgM and virus
positive for months; therefore, timing is less critical for individuals suspected of
having CRS or CRI.[26]
Alternative specimens, such as dried blood spots (DBS) and OF, have recently
been shown to be adequate for surveillance of rubella using IgM detection (DBS
and OF) and virus detection (OF).[27] Note that diagnostic kits are usually not
approved for use with DBS, and low IgM levels in OF necessitate the use of
sensitive detection assays.
Amplification of rubella virus RNA directly from a clinical specimen using RT-
PCR is now common. Assays that can reliably detect 3 to 10 copies of rubella
virus RNA are necessary since many specimens have small amounts of rubella
RNA. Real-time and nested RT-PCR assays often have this level of
sensitivity.[28]
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.[29] The presence of these antibodies
along with, or a short time after, the characteristic rash confirms the diagnosis.[30]
 Rubella Vaccine Immunogenetics:
The current live rubella virus vaccine strain licensed for use in the United
States is the RA27/3 strain. It was first isolated from an infected fetus in the
1960s, and further passaged for attenuation through either the WI-38 or MRC-5
Fig 4

9. 9
human diploid cell lines.[31] It is currently administered as a two-dose series in
the U.S. as part of the measles-mumps-rubella (MMR-II) vaccine. RA27/3 elicits
a robust humoral and cellular immune response. As noted above, correlate
protective levels of anti-rubella antibodies are defined as titers at or above 10
IU/ml.70 However, the measurement of rubella-specific humoral immunity using
serum antibodies can result in a false positives due to a previous parvovirus or
Epstein-Barr virus infection, or the presence of Rh factor.[32] Measuring the
response of rubella-specific memory B cells in vaccinees may be an alternative
correlate and might explain protective immunity in those individuals with low
levels of serum antibodies.81 The seroconversion rate after two doses of MMR-II
approaches 99% and antibodies persist for at least 21 years.[33] The high
seroconversion rate of 99% is observed as early as 9-months-old after receiving
the Wistar RA 27/3 live rubella virus vaccine strain.84 With a calculated half-life
of 114 years, rubella-specific antibodies may even persist for an entire
lifetime.[34] Although excellent seroconversion rates are obtained with RA27/3
vaccination, there are limited occurrences of vaccine failure, and this is thought to
arise when preexisting antibodies neutralize the live viral vaccine strain.[35]
 Treatment:
There is no specific treatment for rubella; however, management is a matter of
responding to symptoms to diminish discomfort. Treatment of newborn babies is
focused on management of the complications. Congenital heart defectsand
cataracts can be corrected by direct surgery.[36]
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.[37]
Pregnant women may be treated with antibodies called hyperimmune globulin that
can fight off the virus. This can help reduce your symptoms. However, there’s still
a chance that your baby will develop congenital rubella syndrome. Babies who are
born with congenital rubella will require treatment from a team of specialists. Talk
to your doctor if you’re concerned about passing German measles on to your
baby.[38]

10. 10
 History:
Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann
made the first clinical description of rubella in 1740,which was confirmed by de
Bergen in 1752 and Orlow in 1758.[39]
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".[40] 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.[41]
It was formally recognised as an individual entity in 1881, at the International
Congress of Medicine in London.[42] In 1914, Alfred Fabian Hess theorised that
rubella was caused by a virus, based on work with monkeys.[43] In 1938, Hiro
and Tosaka confirmed this by passing the disease to children using filtered nasal
washings from acute cases.[44]
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.[45] 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. Since no vaccine was yet
available, some popular magazines promoted the idea of "German measles
parties" for infected children to spread the disease to other children (especially
girls) to immunize them for life and protect them from later catching the disease
when pregnant.[46] The virus was isolated in tissue culture in 1962 by two
separate groups led by physicians Parkman and Weller.[47]

11. 11
 Prevention:
Rubella infections are prevented by active immunisation programs using live
attenuated 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 prepubertal 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.[48]
The vaccine is now usually given as part of the MMR vaccine. The WHO
recommends the first dose be 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.[49]
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.[50]
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). It is recommended that all susceptible non-pregnant women of
childbearing age should be offered rubella vaccination.[51] Due to concerns about
possible teratogenicity, use of MMR vaccine is not recommended during
pregnancy. Instead, susceptible pregnant women should be vaccinated as soon as
possible in the postpartum period.[52]

12. 12
 Etymology:
The name rubella is sometimes confused with rubeola, an alternative name for
measles in English-speaking countries; the diseases are unrelated.[53][54] In some
other European languages, like Spanish, rubella and rubeola are synonyms, and
rubeola is not an alternative name for measles.[55] Thus, in Spanish, "rubeola"
refers to rubella and "sarampión" refers to measles.
 Summary:
Rubella remains an important pathogen globally with approximately 100,000
cases of congenital rubella syndrome estimated to occur each year. Rubella
vaccine is highly effective and safe when used across a population and, as a result,
endemic rubella transmission has been interrupted in the Americas since 2009.
Incomplete rubella vaccination programs result in continued disease transmission
as evidenced by recent large outbreaks in Japan and elsewhere. Herein, we
provide current results regarding rubella control, elimination and eradication
policies, and a brief review of new laboratory diagnostics. In addition, we provide
novel information regarding rubella vaccine immunogenetics and review the
emerging evidence of inter-individual variability in humoral and cell-mediated
innate and adaptive immune responses to rubella vaccine and their association
with HLA alleles, haplotypes, and single nucleotide polymorphisms across the
human genome. Finally, we conclude with a call for further research in rubella
vaccine immunogenetics and its ability to inform a vaccinomics-level approach to
novel vaccine candidate development and the need for a next generation vaccine
that is affordable, easy to administer, and does not require a cold chain for optimal
immunogenicity.

13. 13
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