Measles is a serious infectious disease caused by Measles Virus (MV) (Buchanan & Bonthius 2012; CDC 2013a; Dardis 2012; De Vries et al. 2012; Moss & Griffin 2012). MV is highly contagious (Buchanan & Bonthius 2012; CDC 2013a; Dardis 2012; De Vries et al. 2012; Moss & Griffin 2012).
It has been called “the most communicable of childhood exanthems” and “one of the most communicable of all human diseases” (Buchanan & Bonthius 2012). It is almost certain that a non-immune individual will contract measles disease if exposed to MV (CDC 2013a). Outbreaks of measles can occur within a population even if fewer than 10% of people in the population are non-immune to the disease (Moss & Griffin 2012).
Measles does not cause prolonged or latent infections, and there are no human carriers without clinical disease. There are also no animal carriers or non-human reservoirs for MV; rather, MV spread is maintained through acute infections and interlinked measles outbreaks (Moss & Griffin 2012). Those individuals who successfully fight off measles infection through their immune system gain life-long immunity to measles and cannot become infected again if they remain immune-competent (CDC 2013a; De Vries et al. 2012; Moss & Griffin 2012).
Central to the concept of acquired immunity against MV is the humoral immune response, where antibodies against MV are created and memory cells are formed. These memory cells provide life-long immunity (Buchanan & Bonthius 2012; De Vries et al. 2012; Moss & Griffin 2012). The cellular immune response also plays an important role in combating acute measles infection, but the gaining of life-long immunity is a function of activation of the humoral immune system (Buchanan & Bonthius 2012; De Vries et al. 2012; Moss & Griffin 2012). A way in which immunity against MV can be acquired without measles disease is measles vaccination (Buchanan
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& Bonthius 2012; Dardis 2012; De Vries et al. 2012; Moss & Griffin 2012). Measles vaccination will be reviewed fully in chapter 3.
Infants born to immune mothers are typically protected against measles infection by acquiring maternal antibodies. When this passively acquired immunity disappears, infants become susceptible to infection with MV and consequently measles disease (Leuridan et al. 2010; Moss
& Griffin 2012). The maternal antibodies are transferred to the fetus through the placenta, and the duration of protection of the infant after birth is determined by the amount of maternal antibodies, gestational age (preterm birth leads to lower antibody transfer) and rate of decay of antibodies received from the mother (Leuridan et al. 2010). A prospective study compared the duration of maternal antibody protection between two groups of infants (Leuridan et al. 2010).
One group of infants was born to vaccinated mothers (n=87), and another group of infants was born to mothers who had acquired measles immunity through natural infection (n=120). Measles antibodies (IgG) were measured using an ELISA test in mothers (36 weeks/birth) and infants (1 month/3 months/6 or 9 months), and the amount of antibody present for the two groups were compared. They found a good correlation between amount of maternal antibody and amount of fetal antibody. Vaccinated women had lower antibody counts than naturally immune women.
It also seemed that maternal protection waned quicker in the vaccinated group: the median time to loss of maternal protection was 0.97 months for the vaccine group and 3.78 for the natural immunity group. By six months, 99% of the vaccine group infants had lost all maternal immunity and 95% of the natural immunity group had lost maternal immunity. It would therefore appear that maternal immunity is lost fairly rapidly, and more so in infants born to vaccinated mothers.
This study is not without limitations; one of which is that it is not clear how it was ensured that the two comparison groups were similar or how potential confounders were removed. However, this study does provide some important evidence. One is that infants are susceptible to measles disease fairly early on (median 2.61 months for all infants in this study.) The other is that infants born to vaccinated mothers have a much shorter duration of maternal protection than those born to mothers who had acquired passive immunity, a finding which reflects similar ideas from previous studies as cited by the authors.
MV is considered a respiratory virus, and is usually spread from one person to the next through respiratory droplets produced by coughing or sneezing (Buchanan & Bonthius 2012; CDC 2013a;
Dardis 2012; De Vries et al. 2012; Moss & Griffin 2012). Less often it can be spread by small particles aerosols that can float in the air for some periods of time (Moss & Griffin 2012). It is estimated that MV can remain contagious in such particles for up to 2 hours (CDC 2009). The CDC (2009) states that it is highly probable that non-immune persons will become infected when they come in close proximity to someone who is infected, to the degree that about 90% of non-immune people who come close to an infected person will get measles. Persons infected with measles become contagious a number of days before the onset of the rash, when coughing and sneezing is prominent, until a few days after the onset of the rash (Moss & Griffin 2012). For people with normal immune systems, the 4 days before the onset of the rash and the 4 days after the onset of the rash is the time of highest infectivity, where the virus is optimally spread
44 (Buchanan & Bonthius 2012). In those persons with immune compromise, virus shedding can happen for long periods after the rash has come on, however it is not clear to what degree the infectious period is affected by this (Buchanan & Bonthius 2012; Moss & Griffin 2012).
It is generally thought that once MV enters the respiratory system through infected droplets the virus invades the respiratory epithelial cells, and after replicating in these cells it spreads to the local lymphatic tissue (De Vries et al. 2012; Moss & Griffin 2012). After replicating in the lymphatic tissue, it invades the bloodstream to cause a measles viremia. Through the blood stream the virus then spreads to various tissues, such as the lymph nodes, kidneys, liver, and GI tract. In these organs it invades epithelial cells as well as immune cells and replicates. Another model has been suggested based on studies in monkeys, whereby it is thought that MV initially infects lymphocytes and monocytes, and where viral replication occurs mainly in lymphoid organs and tissues (De Vries et al. 2012; Moss & Griffin 2012).
The response of the immune system to MV is substantial and aggressive, including activation of both cellular immunity and humoral immunity (Buchanan & Bonthius 2012; De Vries et al. 2012;
Moss & Griffin 2012). It is the immune response that is mainly responsible for the development of the symptoms that are associated with measles. During the aggressive and forceful immune response to MV, the reaction of the immune system to other pathogens are suppressed, leading to a period of general immune-suppression during and following measles infection. This may last a few weeks up to a number of months after measles infection. The measles-infected person is therefore susceptible to secondary infections by other bacteria and viruses, which contributes greatly to the complications and impact of measles (Buchanan & Bonthius 2012; De Vries et al.
2012; Moss & Griffin 2012).
MV is a member of the family of Paramyxoviruses, of the genus Morbillivirus (Buchanan &
Bonthius 2012; Dardis 2012; De Vries et al. 2012; Moss & Griffin 2012). It is a single-strand RNA virus. MV has two membrane proteins that are of importance within its pathogenesis: a haemaglutinin protein (H-protein) and a fusion protein (F-protein). These proteins facilitate infiltration of host cells by the virus. The H-protein allows binding of virus to host cell by binding to cell receptors and the F-protein allows the membrane of the virus to merge with the membrane of the host cell (Buchanan & Bonthius 2012; Dardis 2012; De Vries et al. 2012; Moss
& Griffin 2012). Viruses with an RNA genome mutate at a high rate, and this usually makes it a challenge to develop an anti-viral agent (Moss & Griffin 2012). However, the membrane proteins of the measles virus remain fairly stable, and this allows immune memory which confers life-long immunity to those who fight off the disease or receive the vaccine. It is specifically thought that the H-protein is important in terms of immune memory; it is relatively stable over time with little antigenic change, and it provokes a strong response from the immune system. Not only is this important when it comes to naturally acquired immunity, but it also provides for the feasibility of preventing measles infection through vaccination (Moss & Griffin 2012).
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