1. Measles in pregnancy
The World Health Organization estimates that measles is responsible for more than 1 million deaths annually worldwide, making it the sixth to seventh largest killer among infectious diseases—it shares this rank with HIV/AIDS.

2. Virology Genus Morbillivirus of the Paramyxovirus family.
Its genome is a single strand of negative-sense RNA, and it carries two proteins required for viral replication with its protein nucleocapsid. During the process of maturation, the nascent virus acquires a lipid bilayer envelope that contains some host and some viral components.
Host cells may be destroyed by viral replication, but some cells can instead become persistently infected.
Viral replication occurs in a number of cell types, such as epithelium, endothelium, and lymphoid cells, including macrophages and monocytes.

3. Pathophysiology
Measles enters by droplets or by fomites through the upper respiratory tract, with initial replication taking place locally and in regional lymph nodes. Then, primary viremia sets in and infects the reticuloendothelial system.
After 5 to 7 days, secondary viremia follows.
An incubation period of 9 to 12 days culminates in fever, upper respiratory symptoms, and pathognomonic Koplik's spots (red spots with bluish to white centers on the buccal mucosa),
followed 1 to 2 days later by a rash that begins on the head and descends to the trunk and limbs.
Invasion of the respiratory, urinary, and gastrointestinal tracts, as well as the CNS, leads to a variety of symptoms. Sequelae can be acute or chronic.

4. Diagnosis Clinical observation
Immunohistochemistry :viral antigens, in the forms of fluorescent antibody-staining cells, in nasal secretions, urine, or skin biopsy specimens.
Histologic or cytologic specimens : multinucleated giant cells suggestive of measles virus infection.
These indicators decline within a few days of the onset of the rash.
Viral RNA :polymerase chain reaction (PCR) testing, Esp in chronic complications
Subacute sclerosing panencephalitis (SSPE), very high IgG levels in the cerebrospinal fluid (CSF).
Serodiagnosis :IgM antibodies in acute serum samples taken 2 to 3 days after the onset of rash & rising IgG antibodies in later samples. Antibodies in CSF demonstrate CNS involvement.
For assessing the level of protection in previously vaccinated in-dividuals, antibody measurement by means of enzyme-linked immunosorbent assay (ELISA) can be useful.

5. Immunity
A single antigenic type of virus is responsible for natural infection, and infection confers lifelong immunity through the serum antibody response.
Antibodies passively transferred at low titers (transplacentally derived or parenterally administered) probably do not prevent measles, but may permit a milder form of the disease.
Transplacental antibodies from mothers with prior natural infection live longer in infants, compared with antibodies from mothers who had measles vaccination.
Passive immunization is used in measles-exposed populations at risk of serious illness, including immunosuppressed or immunodeficient individuals.
It should also be used when protection is needed during pregnancy
After vaccination, declining but protective titers remain for about 18 years, with natural exposure boosting the immune response somewhat

6. complications
diarrhea (9%)
bacterial or viral otitis and pneumonitis (each about 7%)
postmeasles encephalitis, which occurs in 50 to 400 of every 10,000 measles cases(mortality (20%) and risk of permanent neurologic sequelae (20% to 40%)
encephalitis is the most compelling reason for vigorous vaccination campaigns
subacute sclerosing panencephalitis (SSPE):
a delayed sequel of measles seen mainly in children 5 to 10 years of age. It occurs 5 to 7 years after the primary measles infection
(Its early symptoms are personality change, intellectual decline, and inappropriate behavior, followed by progressive mental deterioration and motor dysfunction, culminating in seizures, coma, and death within a few years. The estimated rate of this complication is 0.5 to 2 for every 100,000 cases)

7. Measles in pregnancy
Threefold greater mortality in pregnant women, compared with nonpregnant women.
High rates of fetal loss, although the mechanism appears to be placental compromise rather than fetal damage or viral teratogenicity
Investigators found measles virus antigen in syncytial trophoblast and decidua, but not in the fetus, in a case of fetal death at 25 weeks' gestation.
Prematurity
Maternal hepatitis and pneumonitis
Premature labor
Spontaneous abortion
Stillbirth

8. Vaccination
Live vaccine should not be given during pregnancy. Vaccinated women should not become pregnant for 30 days after vaccination.
Vaccination of her young children will not threaten a pregnant mother
Measles vaccine has an excellent record of safety but may induce some side effects. As many as 45% of those vaccinated develop a temperature of 103°F (39.4°C) or higher, beginning at about 42 days after vaccination. Transient rashes are reported in 5% of patients, while CNS problems occur in fewer than one per million.

9. Management during pregnancy
When a pregnant woman gets measles near the time of delivery, the fetus may become infected at birth or within 12 days after delivery.
Children born to infected mothers who have measles in the last week of pregnancy or first week postpartum should be treated with immune globulin. Immune globulin (0.25 mL/kg IM)
Immunegluboline is also administered to modify the course of measles in the susceptible gravida within 6 days of exposure to the virus. (Between 5 and 9 days after exposure, this treatment will not prevent secondary viremia, but may reduce the severity of disease.)
Bacterial complications should be treated with appropriate antimicrobial therapy, although there is no reliable therapy for measles encephalitis.
Supportive therapy—especially in pregnancy, where symptoms may be exaggerated and may lead to prematurity or loss of the fetus.
Vitamine A